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Author’s Accepted Manuscript

A role of Ficus species in the management of


diabetes mellitus: a review

Ponnuvel Deepa, Kandhasamy Sowndhararajan,


Songmun Kim, Se Jin Park

www.elsevier.com/locate/jep

PII: S0378-8741(17)33368-8
DOI: https://doi.org/10.1016/j.jep.2017.12.045
Reference: JEP11176
To appear in: Journal of Ethnopharmacology
Received date: 11 September 2017
Revised date: 13 December 2017
Accepted date: 30 December 2017
Cite this article as: Ponnuvel Deepa, Kandhasamy Sowndhararajan, Songmun
Kim and Se Jin Park, A role of Ficus species in the management of diabetes
mellitus: a review, Journal of Ethnopharmacology,
https://doi.org/10.1016/j.jep.2017.12.045
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A role of Ficus species in the management of diabetes mellitus: a review

Ponnuvel Deepa, Kandhasamy Sowndhararajan, Songmun Kim, Se Jin Park*

School of Natural Resources and Environmental Sciences, Kangwon National University, Chuncheon 24341, Gangwon-do, Republic

of Korea

taanishadeepa@gmail.com;

sowndhar1982@gmail.com;

perfume@kangwon.ac.kr;

sejinpark@kangwon.ac.kr

*
Corresponding Author: School of Natural Resources and Environmental Sciences, Kangwon National University, 24341

Chuncheon, Republic of Korea, Phone: 82-33-250-6441; fax: 82-33-259-5563


Abstract

Ethnopharmacological relevance: Diabetes mellitus is one of the most common global health concerns, with a rapidly increasing

incidence. A variety of medicinal plants, particularly those belonging to the genus Ficus (Moraceae), and their active compounds have

been used to treat diabetes and related chronic disorders since ancient times.

Aim of the study: The aim of this review is to provide information regarding traditional and scientific knowledge of Ficus species with

antidiabetic activity to researchers.

Materials and methods: A literature search was conducted to obtain information about the antidiabetic properties of Ficus from the

electronic databases. Common and scientific names of various Ficus species were used as keywords for the search, along with the

terms antidiabetic, hypoglycemic and diabetes.

Results: Among the assorted species of Ficus that were included in our search, F. benghalensis, F. carica, F. glomerata, F. glumosa,

F. racemosa, and F. religiosa exhibited remarkable antidiabetic properties with various mechanisms of action. Moreover, Ficus

species are versatile sources of bioactive metabolites such as flavonoids, phenolic acids, tannins, alkaloids, glycosides, coumarins,

triterpenoids, sterols and vitamin E. These extracts and isolated compounds significantly have enhanced insulin secretion and

subsequently reduced blood glucose level in various in vivo studies.

Conclusion: This review summarizes the antidiabetic potentials of the genus Ficus, including pharmacological studies with

mechanisms of action as well as ethnobotanical uses. This review can help inform future scientific research towards the development

of novel antidiabetic drugs.


Keywords:

Antidiabetic, Diabetes, Ficus, Hypoglycemic, Insulin


1. Introduction

Diabetes mellitus is a metabolic disorder of great concern to health officials, and its prevalence is rapidly increasing in

developing and developed countries. The World Health Organization reported that 30 million people were diagnosed with diabetes in

1985. That number increased to 135 million people in 1995, and approximately 300 million people are estimated to be affected by the

year 2025 (WHO, 2016). The number of diabetes mellitus cases is steadily increasing throughout the world, and its major

complications (disability and hospitalization) are posing a significant financial burden (Adams, 2011). Diabetes mellitus is classified

as type 1 diabetes (5 – 10% of cases) or type 2 diabetes (approximately 90% of cases) based on whether it is caused by impairment of

insulin secretion in the pancreas or by increased insulin resistance, respectively (Beidokhti and Jäger, 2017). Hyperglycemia (high

blood sugar levels) is a common phenotype of uncontrolled diabetes and leads to severe damage in multiple organs of the body,

particularly the nerves and blood vessels.

The treatment of diabetes mellitus and its complications are considered to be an important global health issue. Presently,

different kinds of synthetic drugs, such as incretin mimetics, meglitinides, biguanides, sulfonylureas, thiazolidinediones, α-glucosidase

inhibitors, dipeptidyl peptidase-IV inhibitors and sodium/glucose co-transporter 2 (SGLT2) inhibitors, are available for diabetes

mellitus management. While antidiabetics provide some promising results, they also produce various adverse effects (Gacche and

Dhole, 2011). For example, metformin (biguanides) can lead to abdominal discomfort, anorexia or diarrhea, transient nausea, renal

hypoperfusion and lactic acidosis with severe renal impairment. Thiazolidinediones are known to cause anemia, insomnia, headache,

dizziness, gastrointestinal disturbances, weight gain, visual disturbances, haematuria, proteinuria, impotence, and, less commonly,
fatigue, vertigo and hypoglycemia (Campbell and Howlett, 1995; Seltzer, 1989). Sulfonylurea can cause mild headaches, increased

food intake, gastrointestinal disturbances, weight gain, and cardiovascular mortality and other fatal complications. Therefore, it

remains necessary to search for novel antidiabetic drugs to control diabetic disorders without any side effects (Dhawan et al., 2002;

Idris et al., 2003; Lalau et al., 1987; Lalau et al., 1995; Noor et al., 2008).

The identification of active compounds for the management of diabetes mellitus that have minimal or no side effects remains a

major challenge to the biomedical and scientific communities. Various animal models, particularly murine models, have been used not

only to understand regulatory and metabolic activity for the discovery of novel therapeutic drugs but also for genomic studies on target

genes for obesity and insulin resistance (Masiello, 2006; Ree and Alcolado, 2005). Subsequent screening tests on the efficacy and

toxicity of novel compounds were used in order to avoid or minimize side effects in future translational studies (Chattopadhyay et al.,

1997). In recent years, there has been considerable focus on the identification of new, effective and safe therapeutic drugs to treat

diabetic disorders from plant products because of their low cost, availability and rare side effects. In traditional medicine, several

medicinal plants have been used by different global cultures to prevent long-term complications in the management of diabetes.

Approximately 200 pure bioactive compounds from different chemical groups (e.g., phenolic acids, flavonoids, triterpenoids, alkaloids

and carbohydrates) have been isolated from these medicinal plants and possess strong antidiabetic properties as exhibited by their

regulation of glucose levels in the blood (Misbah et al., 2013).

The genus Ficus belongs to the family of Moraceae, comprising approximately 850 species of trees, shrubs, vines and

epiphytes that are widely distributed in tropical and subtropical countries with greatest diversity in South East Asia, tropical South
America and Australia (Donia et al., 2013; Hamed, 2011). The Asian–Australasian region is the richest and most diverse containing

about 500 Ficus species (Singh et al., 2011). Ficus species traditionally provide edible fruits and are used as religious plants, fodder,

medicine, fuel wood, ornamental plants, and hedges for humans. The significance of Ficus plants as spiritual and material resources

has been documented globally (Shi et al., 2014). Numerous Ficus species have been used for various medicinal purposes in Siddha,

Ayurvedic and traditional Chinese medicine (Lansky et al., 2008). Moreover, various pharmacological studies (e.g., anticancer, anti-

inflammatory and antidiabetic activities) have been supported by the ethnomedicinal uses of Ficus species (Lansky et al., 2008).

Different organs from various Ficus species have long been used by indigenous people throughout the world to effectively

treat diseases, especially diabetes. In the past decades, a number of studies reported that the crude extracts and isolated compounds

from various Ficus species (especially, F. benghalensis, F. religiosa, F. glumosa, F. deltoidea, F. racemosa and F. carica) showed a

potent antidiabetic properties under in vitro and in vivo models. These Ficus species showed protective effect against streptozotocin-

and alloxan-induced diabetic animals and also alleviated all the diabetic-related complications by inducing insulin secretion, inhibiting

glucose absorption, increasing glucose uptake and enhancing pancreatic β-cell levels (Farsi et al., 2014; Irudayaraj et al., 2016;

Ravichandra and Paarakh, 2014a). In this review, we summarize the published scientific reports and ethnobotanical knowledge on the

antidiabetic properties of various Ficus species (Tables 1 and 2). This review also provides sufficient knowledge to researchers in

relation to the underlying mechanisms of the antidiabetic actions of extracts and bioactive components (Fig. 1).

2. Diabetes and its complications


Diabetes is the most important metabolic disease characterized by hyperglycemia in either fasting or postprandial states

resulting from impaired insulin secretion or sensitivity. Diabetes can be classified into type 1, type 2, and gestational diabetes. The

majority of diabetes cases fall into two broad etiopathogenetic categories such as type 1 and type 2 diabetes (Wang et al., 2016). The

main cause of type 1 diabetes is an absolute deficiency of insulin secretion due to the degeneration of pancreatic β-cells. And the cause

of type 2 diabetes is a combination of inadequate insulin secretion and resistance to insulin action in peripheral and liver tissues

(Adams et al., 2011; Inzucchi and Sherwin, 2005). The disruption in the uptake of glucose in skeletal muscle, glucose production by

the liver, and lipid metabolism plays a major role in insulin resistance (Arulselven et al., 2014; Wang et al., 2016). On the other hand,

high blood glucose level is first recognized during pregnancy is called as gestational diabetes (Pedersen et al., 2017).

A variety of factors including family history, obesity, age, and poor dietary and physical exercise habits are responsible for the

development of diabetes mellitus. The acute and chronic complications of diabetes are mainly associated with type 1 or type 2

diabetes. The high blood glucose (hyperglycemia), low blood glucose (hypoglycemia), and ketoacidosis are the acute diabetes

complications. Chronic hyperglycemia state is mainly responsible for the chronic diabetes complications such as retinopathy,

nephropathy, neuropathy, coronary artery disease, peripheral arterial disease, and stroke (Adams et al., 2011; Ding et al., 2010; Forbes

and Cooper, 2013).

3. Mechanisms of antidiabetic activity


Enhancement of glucose utilization in muscle, up-regulation of glucose transporters, enhancement of fat accumulation,

activation of nuclear reporters, and reduction of hepatic glycogen are regarded as important mechanisms for controlling diabetes

complications (El-Abhar and Schaalan, 2014; Tabatabaei-Malazy et al., 2012). The underlying mechanisms of the antidiabetic agents

that have been investigated include the inhibition of glucose absorption in the intestinal tract, increased glucose uptake in skeletal

muscle, and regulation of the glucose homeostasis and antioxidant activity.

3.1. Inhibition of glucose absorption in the intestinal tract

In food consumption, the most important dietary carbohydrates are starch and sucrose, and overconsumption may cause

postprandial hyperglycemia, hyperinsulinemia and other hormonal and metabolic disturbances. -Amylase and -glucosidase are key

enzymes that respond to the digestion of dietary carbohydrates into glucose (Kazeem et al., 2013). Elevated glucose concentration in

the blood induces the secretion of insulin from the pancreatic β-cells, which mediate the uptake of glucose in peripheral tissues

including skeletal muscle and adipose tissue. Subsequently, insulin promotes storage of glucose in the liver as glycogen and inhibits

lipolysis in adipose tissue.

The inhibition of carbohydrate-hydrolyzing enzymes such as -amylase and -glucosidase is important for reducing the rate of

glucose absorption. Plant extracts are potent inhibitors of the intestinal tract enzymes α-glucosidase and α-amylase (Ramirez et al.,

2012). Previous studies have reported that phytoconstituents such as kaempferitrin, quercetin, rutin, kaempferol, pycnogenol,

cyanidin-3-galactoside and cyanidin-3-glucoside highly influence the digestion, absorption and metabolism of carbohydrates by
inhibiting -amylase and α-glucosidase (Akkarachiyasit et al., 2010; Hanhineva et al., 2010; Mendes and Bogle, 2015; Pereira et al.,

2011; Rios et al., 2015).

3.2. Enhancement of glucose uptake in skeletal muscle

Insulin resistance in skeletal muscle, adipose tissue and liver plays a pivotal role in type 2 diabetes mellitus. Defects in glucose

transport, insulin receptor signal transduction, glucose oxidation, glycogen synthesis and fatty acid metabolism can cause insulin

resistance (Panunti et al., 2004). Glucose uptake by insulin is mediated through the action of glucose transporter 4 (GLUT4) in

skeletal muscle (Bouche et al., 2004). GLUT4 is expressed mainly by muscle, kidney cell and adipose tissue (Farsi et al., 2014;

Irudayaraj et al., 2016). The insulin signaling pathway leads to increased glucose uptake in muscle and adipose tissue via the binding

of insulin to GLUT4, which activates signaling enzymes such as phosphatidylinositol-3 kinase (PI3K), Akt-serine/threonine kinase,

and subsequently phosphorylated downstream molecules of the insulin receptors (Hanhineva et al., 2010). The high expression of

GLUT4 in skeletal muscle can facilitate glucose uptake and glycogen storage (Richter and Hargreaves, 2013; Stanford and Goodyear,

2014).

Additionally, peroxisome proliferator-activated receptors (PPARs) play an important role in fat accumulation as well as

carbohydrate metabolism and storage in adipose tissue. PPARα, PPARγ and PPARβ are expressed mainly in liver tissue, adipose

tissue and skeletal muscle (Farsi et al., 2014; Keshari et al., 2016). PPARγ effectively ameliorates insulin resistance. PPARγ agonists

induce increased insulin sensitivity, reduced postprandial glucose and fasting plasma glucose, improved pancreatic β-cell function,
increased high-density lipoprotein (HDL) levels, low-density lipoprotein lower (LDL) levels, decreased microalbuminuria and lower

diastolic blood pressure (Larsen et al., 2003). Therefore, the expression of PPARγ plays a relevant role in adipocyte lipid metabolism

and controls the expression of several enzymes secreted from adipose tissue. Phytoconstituents such as kaempferol, quercetin,

kaempferol 3-neohesperidoside, penta-galloyl-glucose and resveratrol are known to effectively enhance glucose uptake by regulating

the mRNA expression of GLUT4, PPARγ and PI3K (Hanhineva et al., 2010).

3.3. Regulation of glucose homeostasis

The liver plays a major role in the regulation of blood glucose level, maintaining stable blood glucose levels two different

ways: either breaking down the glycogen (glycogenesis) or synthesizing glucose from other metabolites such as amino acids, lactate,

pyruvate and glycerol (gluconeogenesis). Glycogen synthase and glucokinase play a key role in the regulation of glycogenesis.

Enzymes such as glucose-6-phosphatase, pyruvate carboxylase and phosphoenolpyruvate carboxykinase are mainly responsible for the

regulation of gluconeogenesis (Hanhineva et al., 2010). Down-regulation of phosphoenolpyruvate carboxykinase and glucose-6-

phosphatase expressions is responsible for the inhibition of hepatic glucose production by increasing insulin secretion in the pancreas.

Therefore, the balance between glycogenesis and gluconeogenesis is important in the management of diabetic mellitus.

Skeletal muscle also plays an important role in maintaining glucose homeostasis. In the skeletal muscle, insulin promotes

glucose uptake by activating PI3K and Akt, leading to increased translocation of GLUT4 to the plasma membrane. Various bioactive
compounds effectively enhance glucose uptake in skeletal muscle by activating AMP-activated protein kinase (AMPK) (Yagasaki,

2014). AMPK activation promotes insulin sensitivity and regulates the mitochondrial function. AMPK also plays a key role in the

regulation of carbohydrate and fat metabolism. High glucose-induced insulin levels, reduced lipid accumulation, suppressed fatty acid

synthesis and stimulated fatty acid oxidation were all promoted through the AMPK activation pathway. Moreover, the activation of

the AMPK pathway increases the number of pancreatic β-cells and promotes insulin secretion (Mendes and Bogle, 2015).

3.4. Antioxidant activity

It is well known that oxidative stress is highly associated with diabetes mellitus (Arunachalam and Parimelazhagan, 2013;

Mahboob et al., 2005). Non-enzymatic glycation of proteins, glucose degradation and subsequent oxidative degradation can over-

produce free radicals (Mahboob et al., 2005). Diabetes is directly correlated with changes in lipid peroxidation levels and those of

antioxidant enzymes such as superoxide dismutase (SOD), catalase and glutathione peroxidase (Latha and Pari, 2003). Increased

levels of antioxidant enzymes with decreasing levels of lipid peroxidation is an important mechanism to reduce the risk of diabetic

complications (Kamalakannan and Prince, 2006). When diabetic complications arise, tissue damage caused by free radicals through

peroxidation of lipids can lead to extensive membrane damage and dysfunction (Alfy et al., 2005; Ravi et al., 2004). Several

phytochemicals inhibit oxidative stress, which can induce endothelial dysfunction, apoptosis of pancreatic β-cells, systemic

inflammation and decreased glucose uptake in peripheral tissues, promoting plasma glucose reduction (Gothai et al., 2016). Rios et al.
(2015) reported that various natural products significantly improved β-cell function and insulin secretion by suppressing oxidative

stress via antioxidant activity. For example, curcumin, cyanidin-3-O-β-D-glucopyranoside, berberine and other antioxidant rich

extracts showed significant protective effects against oxidative damage in streptozotocin-induced diabetic rats.

4. Antidiabetic potential of Ficus species

Alloxan and streptozotocin are mainly used to induce diabetes disease in animals in antidiabetic studies. Alloxan is derived

from uric acid and selectively injures the pancreatic β-islets, resulting in insulin deficiency, hyperglycemia and ketosis. Similarly,

streptozotocin directly affects pancreatic β-cells via cytotoxic actions, subsequently causing hyperglycemia (Patel et al., 2012). In

various experiments, extracts and compounds isolated from Ficus species effectively ameliorated the alloxan- and streptozotocin-

induced diabetic complications (regulating blood glucose level) in animal models with different mechanisms of action (Table 1; Figs.

1 and 2). Figs. 3 and 4 show the maximum dose range used for the antidiabetic potential of bark, leaf and isolated compounds from

different Ficus species.

4.1. F. amplissima Sm.

F. amplissima is widely distributed in India, northern Australia and other Asian countries (Murugan et al., 2012). In Ayurvedic

medicine, F. amplissima bark is used as a major ingredient for preparing herbal medicines to treat diabetes disorder. The leaves are

used for the treatment of jaundice, the fruit is used to treat mental disturbances and the latex is to cure wounds (Pulliah, 2002; Singh
and Himadri, 2005). In Sri Lankan Siddha medicine, the bark of this plant is used to treat diabetes (Sathasivampillai et al., 2017). The

bark of this plant contains various bioactive components such as lup-20(29)-en-3-yl acetate, lupeol, myristic acid, ergost-5-en-3-ol, β-

stigmasterol, stearic acid, phytol, sitosterol, lanosterol acetate (Murugan et al., 2012). Arunachalam and Parimelazhagan (2013)

studied the antidiabetic effect of different solvent extracts (petroleum ether, chloroform, acetone, methanol and hot water) from the

bark of F. amplissima and found that methanol extract showed a significant blood glucose lowering effect in streptozotocin-induced

diabetic rats. Further, the methanol extract effectively reduced the serum triglyceride and total cholesterol levels and increased serum

insulin level. In the acute toxicity study, F. amplissima bark (up to 2000 mg/kg body weight) treated animals did not show any

changes in the behavioral pattern, the body weight, and food consumption when compared with the control group.

4.2. F. arnottiana (Miq.) Miq.

F. arnottiana bark is traditionally used for the treatment of various disorders including inflammation, diarrhea, diabetes,

burning sensation, leprosy, ulcer, scabies, wounds and skin diseases. Sterols, alkaloids, carbohydrates, tannins and phenolic

compounds are present in the bark extracts. (Babu et al., 2017; Singh et al., 2013). Mazumder et al. (2008) reported that the

component, ficanone isolated from the bark of F. arnottiana exhibited a potent antidiabetic property in streptozotocin-induced diabetic

rats by decreasing oxidative stress in diabetic pancreas and liver as well as increasing insulin secretion from the pancreatic β-cells and

peripheral glucose utilization. Further, ficanone treatment significantly inhibited the carbohydrate intake from intestine and peripheral
glucose release. The results of acute oral toxicity studies showed that the lethal dose of F. arnottiana bark extract (LD50 value) was 3

g/kg body weight.

4.3. F. asperifolia Miq.

F. asperifolia is mainly found in African countries including Senegal, Uganda, Tanzania, South Africa, Madagascar,

Cameroon and Northern Nigeria (Watcho et al., 2009). F. asperifolia leaf extract is used as an anthelmintic and a purgative in African

traditional medicines (Ngadjui et al., 2013). In addition, this plant has various medicinal properties including anticancer, diuretic,

abortificient, ecobolics, and general pain reliever. The leaves are used to treat diabetes by Igala tribe of Logas and Kogi state in

Nigeria (Gbolade, 2009). Further, alkaloids, saponins, tannins, cardiac glycosides, terpenes, steroids, balsam and phenolic compounds

are present in the aqueous leaf extract of this plant (Momoh et al., 2017). Adjanahoun et al. (1996) reported that the aqueous stem

extract of F. asperifolia has hypoglycemic and hypolipidemic properties in diabetic rats. In alloxan-induced diabetic albino rats,

aqueous extract from the stem and bark of F. asperifolia effectively decreased the blood glucose, serum triglyceride and total

cholesterol levels. In addition, the extract significantly increased the serum AST activity and the total protein content (Omoniwa and

Luka, 2012; Omoniwa et al., 2014). Ojo et al. (2016) reported that the oral administration of F. asperifolia aqueous extract did not

show any adverse effect in rats up to the dose of 4000 mg/kg body weight.

4.4. F. benghalensis L.
F. benghalensis is an important medicinal plant, especially in Bangladesh, India and Sri Lanka. In Ayurveda, this plant is used

to treat diarrhea, dysentery and piles, teeth disorders, rheumatism, skin disorders and diabetes (Govindarajan et al., 2011). Extracts and

raw parts of stem bark, fruit and fresh prop root tips have been used to decrease high blood glucose level in Pakistan (Khan et al.,

2011). The mature and raw part of F. benghalensis leaf is used for the treatment of diabetes in rural and urban areas of Dhaka,

Bangladesh (Ocvirk et al., 2013). The decoction obtained from the bark, stem and leaves used for the management of diabetes in

Jammu and Kashmir, India (Bhatia et al., 2014). In Sri Lankan Siddha Medicine, the bark and root are used to control diabetes in the

form of Suravappidippaanundai, Piramehakkulihai and Kudineer (Sathasivampillai et al., 2017). Further, the raw milky latex is used as

diabetes medication inChitta hills of Pothwar region, Pakistan (Arshad et al., 2014). This plant contain various group of bioactive

compounds such as sterols, ketones, flavonoids, triterpenes, furocoumarins and tiglic acid esters (Mandal et al., 2010). The bark

contains tannins, wax, esters and glucoside, 20-tetratriaconthene-2-one, 6-heptatriacontene-10-one, pentatriacontan-5-one, β-sitostirol-

α-D-glucose, meso-inositol, 5,7-dimethyl ether of leucoperalgonidin- 3-0-α-L-rhamnoside, 5,3-dimethyl ether of leucocyanidin, 5,7,3-

trimethoxy leucodelphinidin and 3-O-α-L-Rhamnoside (Taur et al., 2007).

F. benghalensis is one of the most extensively studied medicinal plants for the management of diabetes, especially the bark has

been evaluated in various diabetes animal models by inducing alloxan and streptozotocin. Ahmed et al. (2011) found that the aqueous

extract of bark showed a strong in vitro inhibitory activity against α-amylase and α-glucosidase enzymes. The ethanol extract of leaves

effectively reduced the blood glucose, triglycerides and cholesterol levels in alloxan-induced diabetic rats (Saraswathi et al., 2013). In

streptozotocin-induced diabetic rats, bark aqueous extract and an isolated compound, α-amyrin acetate exhibited antidiabetic activity
by decreasing the blood glucose level and increasing the HDL level (Singh et al., 2009a; 2009b). Further, aqueous extract of bark

significantly restored the fasting blood glucose level and enhanced glucose tolerance in alloxan-induced diabetic rats (Gupta et al.,

2002). In another study, the aqueous extract of bark effectively decreased the blood glucose level and restored microsomal protein

concentration and cytochrome P-450 dependent monooxygenase enzymes (EROD, PROD and PNPH) in streptozotocin-induced

diabetic rats. In addition, the extract reduced the inflammation and swelling in pancreatic tissue (Gayathri and Kannabiran, 2008).

Saifi et al. (2014) reported that hydro alcoholic extract of bark effectively reduced the blood glucose level and serum cholesterol,

triglycerides, LDL, creatinine, urea, alkaline phosphatase, bilirubin, glutamate oxalate transaminase and glutamate pyruvate

transaminase levels. Further, the hydro alcoholic extract increased the HDL and albumin levels. Augusti et al. (1994) found that

leucopelargonidin-3-0-α-L rhamnoside isolated from the bark of F. benghalensis (at 100 mg/kg) exhibited antidiabetic potential in

alloxan-induced diabetic dogs. The ethanol extract and isolated compounds (leucodelphinidin, leucoanthocyanidia and

leucoanthocyanin) from the bark of F. benghalensis effectively controlled the hypoglycemia and hyperglycemia in rabbits and rats

(Bramachari and Augusti, 1961; 1964; Geetha and Mathew, 1994). Akanksha et al. (2010) reported that α-amyrin acetate isolated

from the aerial root significantly decreased blood glucose level in streptozotocin induced diabetic rats. In alloxan-induced diabetic

rabbits, the aqueous extract of bark effectively decreased the serum cholesterol, low density lipoprotein cholesterol, triacylglycerol,

glycosylated haemoglobin, blood glucose level (Shukla et al., 1995). The ethanol extract of fruit also controlled diabetes by reducing

the blood glucose and total cholesterol levels in alloxan-induced diabetic rats (Priya et al., 2013). In acute toxicity studies, no mortality
and signs of toxicity were observed at the dose of 2000 and 5000 mg/kg body weight for aqueous and ethanol extracts, respectively

(Patil et al., 2010a; 2010b).

4.5. F. carica L.

F. carica is a deciduous tree, native to Asia Minor, and widely found in tropical and sub-tropical countries (Anonymous,

2002). This plant has been used to treat diabetes, liver diseases, asthma, cough, ulcer, vomiting, menstruation pain, skin diseases,

scabies, and gonorrhea. (Badgujar et al., 2014). The boiled root of F. carica has been used as a medication against diabetes by Bapedi

healers in Limpopo Province, South Africa (Semenya et al., 2012). In Morocco, fruits and leaves are used to treat diabetes

complications (Barkaoui et al., 2017; Tahraoui et al., 2007). The decoction of leaves also used for controlling diabetes in Pakistan

(Mopuri and Islam, 2016). Previous studies reported the presence of bioactive metabolites such as triterpenoids, steroids, coumarins,

and flavones in fruits, leaves, and stem of F. carica (Jain et al., 2013). In F. carica fruits, 6-O-acyl-β-D-glucosyl-β-sitosterols along

with its palmitoyl, linoleyl, stearyl and oleyl derivatives were isolated (Gilani et al., 2008). Psoralen, bergapten, quercetin 3-O-

rutinoside, ferulic acid, 3-O-caffeoylquinic acid and 5-O-caffeoylquinic acid were isolated from the leaves (Mahmoudi et al., 2016).

Different extracts of fruits and leaves showed a potent inhibitory activity against α-amylase and α-glucosidase enzymes

(Mopuri and Islam, 2016; Mopuri et al., 2017; Wojdylo et al., 2016). In a human study, the decoction of leaves effectively controlled

postprandial glycemia (Serraclara et al., 1998). Ficusin isolated from the leaves of F. carica remarkably decreased the blood glucose

level and improved lipid profile, plasma insulin, nephritic marker, liver glycogen, liver enzymes and protected β-cells. In the
antidiabetic mechanism, ficusin effectively upregulated PPARγ and activated the glucose transport through translocation and GLUT4

activation in adipose tissue (Irudayaraj et al., 2016). Further, aqueous and chloroform extracts from the leaves of F. carica, exhibited

antidiabetic activity in streptozotocin-induced diabetic rats (Perez et al., 2000; 2003). El-Shobaki et al. (2010) reported that raw fruits

and leaves of F. carica showed a strong antidiabetic activity in alloxon-induced diabetic rats by increasing antioxidant levels. In

addition, methanol and ethanol extracts from the leaves of F. carica significantly decreased the blood glucose level in alloxan-induced

diabetic rats (Jayakumar et al., 2014; Stalin et al., 2012). The fruit of this plant also possessed antidiabetic activity in streptozotocin-

induced albino Wistar rats (Sheikh et al., 2015). The methanol extract of fruits, aqueous extract of leaves and decoction obtained from

the leaves also controlled the diabetic complications in streptozotocin-induced diabetic rats (Canal et al., 2000; Rashidi and

Noureddini, 2011; Sheikh et al., 2015). Further, the aueous extract of F. carica leaves showed negative behavioural changes in rats at

5000, 5500, 5750 and 6000 mg/kg dosages, but mortality was not observed up to the dose of 6000 mg/kg body weight (Odo et al.,

2016).

4.6. F. dalhousiae Miq.

F. dalhousiae is a small spreading tree and endemic to peninsular region. Leaves and bark are traditionally used to cure liver

and skin diseases. Further, bark is used for the treatment of cancer and hyperlipidemia (Ghori et al., 2015; Pasha, 2014). F. dalhousiae

leaves possess antioxidant, antihyperglycemic and gastroprotective properties (Surya et al., 2017). Ghori et al. (2014a) found that

ethanol extract of F. dalhousiae leaves effectively maintained the blood glucose level and increased the level of plasma insulin in
alloxan-induced diabetic rats. Ghori et al. (2014b) found that the ethanolic extract of F. dalhousiae root did not show any mortality up

to the dose of 2000 mg/kg body weight.

4.7. F. deltoidea Jack

F. deltoidea is an epiphytic shrub and mainly distributed in Peninsular Malaysia, Thailand, Java, Borneo, Sumatra and

Moluccas (Berg and Corner, 2005). Fruits are used to treat headache, toothache and cold. The stem and bark of F. deltoidea are used

to treat various disorders such as pneumonia, diabetes mellitus, high blood pressure, skin disease and gout (Ong et al., 2011). In

traditional systems of medicine, the decoction obtained from leaves of F. deltoidea is used to treat diabetes, contract the uterus and

vaginal muscles, the menstrual cycle disorders, and leucorrhoea (Bunawan et al., 2014; Forest et al., 2003). In Singapore, the raw

leaves have been used for the management of diabetes (Siew et al., 2014). Previous studies revealed the presence of flavonoids

isovitexin, vitexin, proanthocyanidins, flavan-3-ol monomers and flavones glycosides in F. deltoidea. F. deltoidea leaves have various

pharmacological properties such as antidiabetic, antinociceptive, antiulcer, antioxidant, anti-inflammatory and antimelanogenic

activities (Misbah et al., 2013).

In a clinical study, aqueous extract obtained from the leaves of F. deltoidea (at 1000 mg) significantly decreased the total and

LDL cholesterol levels in healthy adults with pre-diabetes (aged 21 to 65) (Kalman et al., 2013). Further, vitexin and isovitexin

isolated from the leaves restored the blood glucose level in streptozotocin-induced diabetic rats (Choo et al., 2012). Adam et al. (2012)

evaluated the antihyperglycemic mechanisms of F. deltoidea leaves using BRIN BD11 cell line and reported that the hot aqueous
extract stimulated the insulin secretion effectively than ethanol and methanol extracts. Ilyanie et al. (2011) studied the antidiabetic

effect of methanol, aqueous, n-hexane, chloroform and n-butanol extracts of leaves. The authors found that the methanol extract

exhibited a potent blood glucose lowering activity in mildly insulin resistant diabetic rats as well as in normoglycemic mice. In

another study, the methanol extract of F. deltoidea leaves stimulated insulin secretion and blocked hepatic glucose production by

down-regulating phosphoenolpyruvate carboxykinase and glucose-6-phosphatase expressions and up-regulating hepatic GK and

PPARγ expressions. Further, the methanol extract significantly increased GLUT-4 gene expression in skeletal muscles (Farsi et al.,

2014). In addition, oral administration of ethanol extract of F. deltoidea leaves to diabetic rats resulted in a significant reduction of the

blood glucose level (Noor et al., 2016). In acute toxicity studies, the methanol extract from the leaves of F. deltoidea found to be safe

at the dose level of 5000 mg/kg (Farsi et al., 2014). Ilyanie et al. (2011) also reported that there were no adverse effect and mortality in

diabetic rats administered with methanol extract of leaves up to the dose of 6400 mg/kg.

4.8. F. exasperata Vahl

F. exasperata (sand paper tree) is a deciduous shrub and widely distributed in Nigeria. The leaf extract of this plant has been

traditionally used to treat hypertension, heamostative opthalmia, coughs, bleeding, diarrhea and haemorrhoid (Akanni et al., 2014; Ijeh

and Ukweni, 2007). The leaf and stem extracts contain flavonoids, tannins, saponins, alkaloids and cyanogenic glycosides (Hallan,

1999; Ijeh and Agbor, 2006). The decoction obtained from the leaf, root, bark and latex has been used to treat diabetes complications

in various locations across Nigeria (Abo et al., 2008; Ezuruike and Prieto, 2014; Shinkafi et al., 2015).
Previous studies reported that the leaves of F. exasperata have various pharmacological properties such as anti-inflammatory,

antiarthritic, antinociceptive, anticonvulsant, anxiolytic, antiulcer, antipyretic, and antimicrobial activities. In Nigeria, F. exasperata

leaves are mainly used for the management of diabetes and hypertension in addition to the treatment of topical wounds (Ahmed et al.,

2012; Umeh et al., 2014). The scientific studies revealed that the aqueous extracts from the leaves of F. exasperata showed

antidiabetic activity in streptozotocin- and alloxan-induced diabetic rats (Adewole et al., 2011; 2012; Adeyi et al., 2012). Another

study indicated that the aqueous extract of leaves effectively ameliorated glucose intolerance in fructose-induced rats (Taiwo et al.,

2010). In addition, no adverse effect or mortality was observed at 2.5, 5, 10 and 20 g/kg oral administration of aqueous extract of

Ficus exasperata leaves (Bafor and Igbinuwen, 2009).

4.9. F. glomerata Roxb.

F. glomerata is a moderate-sized to large tree and occurred in India and Southeast Asia. In traditional systems of medicine, F.

glomerata has been used for the treatment of diabetes, liver diseases, piles, asthma, leprosy and diarrhea. In particular, the bark, fruits

and latex are used to cure anemia, constipation and dysentery (Chopra et al., 2002; Verma et al., 2010). F. glomerata plant extracts

have been reported to possess various bioactive constituents including flavonoids, carbohydrates, alkaloids, tannins, glycosides,

saponin and steroids. (Hogade et al., 2015). The stem bark of F. glomerata contains β-sitosterol, leucocyanidin-3-O-β-D-

glucopyrancoside, leucopelargonidin-3-O-β-D-glucopyranoside, leucopelargonidin-3-O-α-L-rhamnopyranoside, lupeol, ceryl


behenate, lupeol acetate, α-amyrin acetate, leucoanthocyanidin and leucoanthocyanin and stigmasterol. Glauanol acetate and

racemosic acid were isolated from the leaves (Rumzhum et al., 2012).

In alloxan-induced diabetic rabbits, the aqueous extract of F. glomerata leaves effectively reduced the blood glucose level and

increased the insulin secretion (Akhtar and Qureshi, 1988). The ethanol extract from the leaves significantly reduced the blood

glucose, serum urea, creatinine and cholesterol levels in alloxan-induced diabetic rats (Sharma et al., 2010). In addition, methanol

extract obtained from the bark exhibited antidiabetic activity in alloxan-induced diabetic rats (Heroor et al., 2014). Further the

authors found that no mortality or behavioral changes were observed in rats up to the dose of 2000 mg/kg body weight.

4.10. F. glumosa Delile

F. glumosa is an important medicinal plant, extensively used for the treatment of edema, hemorrhoid, cardiovascular diseases,

hypertension, skin diseases and diabetes in Cameroon, Senegal and East Africa (Madubunyi et al., 2012). F. glumosa contains

flavonoids, saponins, carbohydrate, tannins, and triterpenes (Ntchapda et al., 2014). The stem, leaves, bark of this plant is used as

diabetes medications in African countries (Olaokun et al., 2013; Madubunyi et al., 2012). Madubunyi et al. (2012) studied the in vitro

antioxidant and in vivo antidiabetic potential of the methanol extract of F. glumosa stem bark in alloxan-induced diabetic mice. The

methanol extract of F. glumosa stem bark showed a promising antidiabetic effect in alloxan-induced hyperglycemic rats (Onoja et al.,

2014). Umar et al. (2013) investigated the effect of ethanol extract of F. glumosa leaves on fasting blood glucose and serum lipid

profile in diabetic rats. In another study, ethanol extract of F. glumosa leaves significantly decreased the fasting blood glucose level
and increased the levels of liver enzymes [aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline

phosphatase (ALP)] in alloxan-induced diabetic rats (Usman and Mohamed, 2015). The acute toxicity study reaveled that the

methanol extract of F. glumosa leaves found to be safe at the dose range from 200–2,500 mg/kg (Madubunyi et al., 2012).

4.11. F. hispida L.f.

F. hispida is mainly distributed in Asian countries and Australia (Berg and Corner, 2005). This plant is traditionally used to

treat several ailments such as ulcers, psoriasis, anemia, dysentery, piles, diabetes and jaundice (Ali and Chaudhary, 2011; Anand et al.,

2015). The raw and matured fruit of this plant has been used to treat diabetes by Sugali tribal inhabitants of Yerramalais in Kurnool

district, Andhra Pradesh, India and Santal tribe in Rangpur district, Bangladesh (Basha et al., 2011; Rahmatullah et al., 2010a). In

addition, sap obtained from the root has been used as a diabetes medication by rural community of Dhemaji district of Assam,

Northeast India (Ghosh et al., 2004; Tarak et al., 2011). Leaves and seed of F. hispida have also been used to control diabetes in

Kavirajes of Chalna area, Khulna district, Bangladesh (Rahmatullah et al., 2010b). Twigs of F. hispida contain ficushispimines A and

B, ficushispimine C, and ficushispidine. Hispiloscine is present in the stem bark and leaves. Further, the F. hispida bark contains ??-

amyrin acetate, N-triacontanyl acetate, lupeol acetate, and 10-ketotetracosyl arachidate (Howlader et al., 2017).
Ghosh et al. (2004) reported that the ethanol extract of F. hispida bark effectively reduced the fasting blood glucose level and

increased glycogen content of the liver, skeletal and cardiac muscles in alloxan-induced diabetic rats. The methanol extract from the

leaves of F. hispida showed a potent antidiabetic activity in alloxan-induced diabetic rats by reducing blood glucose, serum SGOT,

triglycerides and cholesterol levels (Ravichandra and Paarakh, 2014a). Further, the methanol extract of leaves significantly reduced

the serum glucose level in glucose loaded mice (Shahreen et al., 2012). Moreover, the single dose of 2000 mg/kg of methanol extract

of leaves did not produce any mortality or behavioral changes in the tested animals (Ravichandra and Paarakh, 2014a).

4.12. F. microcarpa L.f.

F. microcarpa is distributed in India, Southern China, Yukyu Islands, Australia and New Caledonia. The aerial root of F.

microcarpa has been traditionally used for the treatment of perspiration, deintoxication, fever, pain, and heat in China, Vietnam and

Okinawa Islands (Ya et al., 2010). The bark, fruits and leaves of F. microcarpa have been used to treat diabetes complications in

Pakistan and Tamil Nadu, India. In South Asia, this plant has been used as folk medicine to cure type-2 diabetes (Jayachandran and

Mahesh, 2007; Khan et al., 2011). It was reported that F. microcarpa aerial root contains polyphenols, organic acids, alkaloids and

polysaccharides (Jiang et al., 2014). Megastigmanes, pheophytins, catechin, epicatechin and isovitexin are found in leaves of F.

microcarpa and bark contains phenolic acids (Chan et al., 2017). The methanol and ethanol extracts of F. microcarpa leaves showed

protective effect against alloxan-induced diabetic rats by reducing blood glucose, cholesterol and triglycerides levels and increased
insulin level. Further, the oral administration of a single dose of 2000 mg/kg ethanol or methanol extract of leaves showed no

mortality or behavioral alterations in the tested animals (Kumar et al., 2007; Ravichandra and Paarakh, 2013).

4.13. F. nervosa B.Heyne ex Roth

F. nervosa is a moderate-sized evergreen tree. Traditionally, the leaves are used for the treatment of diabetes and rheumatism

(Raj et al., 2011). 3-Hydroxyxanthyletin, 3-methoxyxanthyletin, xanthyletin, umbelliferone, scopoletin, β-(S)-marmesin and other

bioactive compounds were identified in this plant (Chen et al., 2010). The ethanol and ethyl acetate extracts from the leaves of F.

nervosa attenuated diabetic complications by decreasing the blood glucose, serum urea, creatinine and cholesterol levels and

increasing the protein level in alloxan-induced diabetic rats (Devi et al., 2012). Raj et al. (2011) found that the petroleum ether extract

from the leaves of this plant reduced serum glucose, total cholesterol, and triglycerides levels in streptozotocin induced diabetic rats.

The authors also reported that there were no signs of toxicity and mortality in rats administered with petroleum ether extract of leaves

up to the dose of 2000 mg/kg.

4.14. F. palmata Forrssk

F. palmata is widely found in Nepal, India, Pakistan, Afghanistan, Iran, Arabian Peninsula, Somalia, Sudan, Ethiopia and S.

Egypt. The raw fruit of this plant has been used to cure diabetes in Pothwar region, Pakistan (Arshad et al., 2014). Psoralene, trans-

psoralenoside, germanicol acetate, bergapten, vanillic acid and rutin were isolated from F. palmata (Alqasoumi et al., 2014). Further,
gallic acid, ellagic acid, β-sitosterol, sigmasterol and glaunol acetate, ceryl behenate, lupeol, α-amyrin, β-amryin acetate were isolated

from leaves, bark and heartwood of F. palmata (Singh et al., 2014). In streptozotocin-induced diabetic rats, the hydroalcoholic extract

obtained from the leaves of F. palmata effectively reduced the blood glucose, serum triglyceride and total cholesterol levels and

increased serum insulin, body weight and glycogen content in liver and skeletal muscle. Further, the acute toxicity study exhibited that

the extract found to be safe in rats up to the dose of 2000 mg/kg (Singh et al., 2014).

4.15. F. platypoda (Miq.) A.Cunn. ex Miq.

F. platypoda (desert fig or rock fig) is endemic to central, northern Australia, and Indonesia (El-Kashoury et al., 2013). 3-

Methoxycarpachromene, pheophorbide-a methyl ester, pheophorbide-b methyl ester, 3-oxo-6-hydroxy-α-ionol, β-sitosterol-3-O-β-D-

glucopyranoside and rutin were isolated from F. platypoda leaves (Afifi et al., 2014). El-Kashoury et al. (2013) reported that the

ethanol extract of F. platypoda leaves significantly reduced the blood glucose level in alloxan-induced diabetic rats. The findings of

acute toxicity studies revealed that the ethanol extract of F. platypoda leaves did not produce any behavioral alterations in the tested

animals up to the dose of 2000 mg/kg (El-Kashoury et al., 2013).

4.16. F. pseudopalma Blanco

F. pseudopalma is mainly used for the treatment of kidney stones and diabetes. The decoction of leaves has been used to treat

diabetes in Bicol region, Philippines (Salonga et al., 2013). In the dichloromethane extract from the leaves of this plant, squalene,
polyprenol, β-amyrin fatty acid ester, α-amyrin acetate, β-amyrin acetate, lupeol fatty acid ester, lupenone, oleane, and ursenone were

identified (Llagas et al., 2014). The hot water extract of leaves showed a strong antidiabetic effect in glucose, maltose and starch

loaded mice (Salonga et al., 2013). Acosta et al. (2013) reported that dichloromethane extract of F. pseudopalma leaves is non-toxic in

rats up to the dose of 2000 mg/kg body weight.

4.17. F. pumila L.

F. pumila is a scandent shrub, indigenous to South China and Malaysia. The leaves of this plant has been traditionally used for

the treatment of diabetes, dizziness, high blood pressure, and neuralgia (Leong et al., 2008; Mitsuhashi, 1988). Based on the

preliminary phytochemical analysis, carbohydrate, glycosides, sterols, flavonoids and triterpenes were present in this plant. Previous

studies reported that F. pumila contains apigenin, luteolin, rutin, genistein, hesperidin, astragalin, isoquercitrin, and chrysin (Ashraf et

al., 2013). The ethanol extract of leaves effectively decreased the blood glucose, LDL, VLDL, TC and TG levels and increased the

HDL level in streptozotocin-induced diabetic rats (Thamotharan et al., 2013). Wu et al. (2017) investigated the antidiabetic potential

of pectic polysaccharide with hexenuronic acid from the fruit of F. pumila using C57BL/KsJ db/db mice. In their study, pectic

polysaccharide treatment ameliorated hyperglycaemia in association with an enhancement in hepatic glycogen metabolism in mice.

Pectic polysaccharide treatment activated insulin receptor substrate-1/phosphatidylinositol-3 kinase/protein kinase B/glycogen

synthase kinase-3β/glycogen synthase insulin signaling pathway and AMP-activated protein kinase/glycogen synthase kinase-3β

/glycogen synthase signaling pathway. In addition, this treatment regulated glucokinase, phosphoenolpyruvate carboxykinase and
glucose-6-phosphatase expressions in hepatic glycogenesis and glycogenolysis. In acute toxicity study, the oral administration of

methanol extract of F. pumila showed no mortality and behavioral alterations in mice at doses of 2.5, 5 and 10 g/kg (Liao et al., 2012).

4.18. F. racemosa L.

F. racemosa is a moderate to large sized spreading tree, without much prominent aerial roots. This plant is widely found all

over India, northern Australia and other parts of Asia (Veerapur et al., 2012). In the traditional systems of medicine, all parts of this

plant (leaves, fruits, bark, latex, and sap of the root) are medicinally important. The decoction of bark is used for treatment of various

disease such as skin diseases, ulcers, diabetes, piles, dysentery, asthma, gonorrhea, gleets, leucorrhea and urinary diseases. The fruit

juice and matured raw fruits have been used as diabetes medications by different tribal communities in India and Bangladesh (Chhetri

et al., 2005; Khan et al., 2015; Mahbubur Rahman, 2015; Ocvirk et al., 2013). In Sri Lankan Siddha Medicine, bark and latex have

been used as diabetes medication in the form of periya kulihai, ayakkaanthakkulihai, suravappidippaanundai, naaval ney,

vachchirasinthaamani irasaayanam, and Kudineer (Sathasivampillai et al., 2017). The root part of this plant also used for the

treatment of diabetes in Javadhu hills, Tamil Nadu, India and Chana and Nathawee district, Songkhla Province, Thailand (Neamsuvan

et al., 2015; Thirumalai et al., 2012).

A number of bioactive compounds have been isolated from different plant parts of F. recemosa. Campesterol, hentriacontane,

hentriacontanol, kaempferol, stigmasterol, methyl ellagic acid were isolated from the stem. Glauanol, hentriacontane, β-sitosterol,

glauanolacetate, esters of taraxasterol, lupeolacetate, friedelin, and other phytosterols were isolated from fruits. Whereas cycloartenol,
euphorbol and its hexacosanoate, taraxerone, tinyatoxin were isolated from the root (Murti and Kumar, 2012). The stem bark of F.

racemosa contains various bioactive compounds such as saponin gluanol acetate, β-sitosterol, leucocyanidin-3-O-β-D-

glucopyrancoside, eucopelargonidin-3-O-β-D-glucopyranoside, leucopelargonidin-3-O-α-L-rhamnopyranoside, lupeol, ceryl behenate,

lupeol acetate, α-amyrin acetate, leucoanthocyanidin, eucoanthocyanin and stigmasterol (Gowda and Swamy, 2011).

The ethanol extract of bark showed a promising antidiabetic effect in alloxan-induced diabetic rats by restoring blood glucose,

lipids and lipoprotein levels to near normal range (Goyal and Jain, 2012; Sachan et al., 2009; Sophia and Manoharan, 2007). In

streptozotocin-induced diabetic rat model, the ethanol extract of F. racemosa bark significantly restored the blood glucose and lipid

levels and reduced the creatinine kinase, blood urea nitrogen, collagen and albumin levels (Joshi et al., 2016; Veerapur et al., 2012).

The methanol extract of bark also showed an antidiabetic effect in Streptozotocin- and alloxan-induced diabetic rats (Bhaskara Rao et

al., 2002; Solanki and Bhavsar, 2015). Tannin obtained from the bark of F. racemosa reversed the increased blood glucose, total

cholesterol, triglycerides, LDL levels in streptozotocin-induced diabetic rats (Velayutham et al., 2012). In another study, tannin

fraction obtained from the acetone extract of bark restored the antioxidant status of the organs to normal levels in addition to reversed

the blood glucose, total cholesterol, triglycerides and LDL levels (Ravichandiran et al., 2012). In a human trial, aqueous extract of

bark effectively reduced the blood glucose level (Gul-E-Rana et al., 2013).

Keshari et al. (2016) investigated the antidiabetic effect of 4 flavonoids (similar to kaemferol, quercetin, naringenin and

baicalein) isolated from the bark of F. racemosa. In their study, the flavonoids effectively reduced the blood glucose level and restored

body weight in streptozotocin-induced diabetic rats. Further, these flavonoids expressed the hypoglycemic action via binding to
PPARγ and GLUTI receptor. The ethanol extract of fruit also exhibited a considerable antidiabetic activity in streptozotocin-induced

diabetic rats and alloxan-induced mice (Jahan et al., 2009; Zulfiker et al., 2011). In alloxan-induced diabetic mice, petroleum ether

extract from the fruit significantly enhanced glucose utilization and effectively reduced the serum glucose level without causing a

hypoglycaemic state (Deshmukh et al., 2007). In addition, sterols from the leaves reduced the blood glucose level and serum lipid

parameters and improved HDL level in streptozotocin-induced diabetic rats (Kushwaha et al., 2015). The ethanol and pertroleum ether

extract of leaves showed a potent antidiabetic effect in sterptozotocin-induced diabetic rats by normalizing the level of SOD, catalase,

glutathione reductase and glutathione peroxidase enzymes and lipid profiles (Yadav et al., 2015). The results of acute toxicity studies

revealed that the ethanol extract of F. racemosa leaves was non-toxic up to the dose of 2000 mg/kg (Patil et al., 2010; Zulfiker et al.,

2011).

4.19. F. religiosa L.

F. religiosa is mainly found in the sub-Himalayan tract, Bengal and central India. The different organs of this tree have been

commonly used for the treatment of various ailments such as diabetes, atherosclerosis, Alzheimer's disease, gastritis, cancer and AIDS

(Sankar et al., 2014). This plant is also used to treat throat diseases, kidney stones, blindness, rheumatism, sprains and fractures,

jaundice, diarrhea, glossitis, miscarriage, indigestion and hernia (Ballabh et al., 2008). The bark, leaves and stem have been used to

control diabetes complications in various countries including India, Sri Lanka and Pakistan (Khan et al., 2011; Olaokun et al., 2013;

Sathasivampillai et al., 2017). The ethanol and methanol extracts of F. religiosa bark were reported to contain lupeol, β-sitosterol, β-
sitosterol-d-glucoside, stigmasterol, lanosterol and campesterol. Whereas petroleum ether extract of bark contain octacosanol, methyl

oleonate and lupen-3- one. In addition, bergapten and bergaptol were found in the benzene extract of bark (Priyanka et al., 2017).

The aqueous extract of bark had a promising antidiabetic effect in streptozotocin-induced diabetic rats by decreasing the blood

glucose, serum triglyceride and total cholesterol levels and increasing serum insulin, body weight and glycogen content in the liver

and skeletal muscle (Kirana et al., 2011; Pandit et al., 2010). The aqueous extract of F. racemosa leaves exhibited an antidiabetic

effect in alloxan-induced diabetic rats by decreasing blood glucose, serum cholesterol and triglyceride levels (Pochhi and

Muddeshwar, 2017). Goswami et al. (2010) investigated the antidiabetic effect of ethanol extracts from the leaves and fruits in

alloxan-induced diabetic rats. The authors found that ethanol extracts decreased the blood glucose level by stimulating β-cells to

release insulin. In a recent study, ethanol extract loaded solid lipid nanoparticles from the stem bark significantly reduced blood

glucose level in streptozotocin-induced diabetic rats (Priyanka et al., 2018). In addition, Pandit et al. (2010) reported that the aqueous

extract of F. racemosa bark was safe up to the dose of 2000 mg/kg.

4.20. F. sycomorus L.

F. sycomorus is mainly distributed in tropical West Africa. In different parts of Africa, stem bark, leaves and root of F.

sycomorus have been used for the management of diabetes (Olaokun et al., 2013). Previous studies reported that the extracts from the

stem bark contain tannins, saponins, flavones, aglycones, anthraquinone glycosides and flavonoid glycosides (Al-matani et al., 2015;

Bekheet et al., 2011). In an in vitro study, the acetone extract of leaves showed a potent inhibitory activity against α-glucosidase
enzyme (Olaokun et al., 2013). Njagi et al. (2012) reported that the aqueous extract of F. sycomorus bark showed a protective effect

against alloxan-induced diabetic mice. It was reported that the methanol extract of F. sycomorous stem bark is non-toxic up to the

dose of 5000 mg/kg (Adoum et al., 2012).

4.21. F. thonningii Blume

F. thonningii tree is indigenous to savannah part of Nigeria. Leaves of F. thonningii are widely used to treat various ailments

including sore throat, colds, diarrhea, jaundice, malaria fever, dysgalactia, gonorrhea and respiratory diseases. The decoction obtained

from the stem bark, leaves and fruits has been used for the management of diabetes in Nigeria and other parts of Africa (Ezuruike and

Prieto, 2014). F. thonningii leaves contain various bioactive metabolites such as anthraquinones, glycosides, flavonioids, alkaloids

steroids, aglycones, tannins, triterpenes and saponins (Ahur et al., 2013; Maiha et al., 2013). Flavone-C-glycosides namely, Orientin,

vitexin and isovitexin were isolated from the leaves of F. thonningii Greenham et al (2007). A study indicated that the ethanol extract

of bark effectively decreased the blood glucose level in streptozotocin-induced diabetic rat model (Musabayane et al., 2007). Aniagu

et al. (2008) found that the LD50 values of F. thonningii leaves were >3000 mg/kg, p.o. and 548 mg/kg, i.p.

4.22. Other Ficus species

Arunachalam and Parimelazhagan (2014) studied the antidiabetic effect of methanol extract of F. talbotii bark using

streptozotocin-induced diabetic rat model. In their study, the methanol extract increased the serum insulin, HDL and plasma enzymes
and glycogen levels in the liver and muscles. In addition, the extract effectively decreased the fasting blood glucose, total cholesterol,

serum triglycerides and serum marker enzymes levels. The HPLC analysis revealed that the presence of rutin, quercetin and kaemfeorl

in this extract. The authors also found that the methanol extract of F. talbotii bark was safe in rats up to the dose of 2000 mg/kg body

weight. Aqueous and ethanol extract from the leaves of F. cyathistipula showed antidiabetic activity in alloxan-induced diabetic rats.

F. cyathistipula leaf extract contians α-amyrin palmitate, lupeol acetate, taraxerol, β-sitosterol, protocatechuic acid and 3-O-caffeoyl

quinic acid (El-Sakhawy et al., 2016).

The ethyl acetate and methanol extracts of F. mollis leaves showed antidiabetic effect in dexamethasone- and alloxan-induced

diabetic rats, respectively. In addition, oral administration of ethyl acetate and methanol extracts of F. mollis showed no mortality or

any signs of toxicity in rats up to the dose of 3000 and 2000 mg/kg, respectively (Munna and Saleem, 2013; Ravichandra and Paarakh,

2014b). The dichloromethane extract from the leaves of F. odorata restored the blood glucose level near to normal in streptozotocin-

induced diabetic rats (Degollado et al., 2014). The acetone extract from the leaves of F. lutea showed a strong inhibitory activity

against α-amylase and α-glucosidase enzymes (Olaokun et al., 2013). Further, Olaokun et al. (2016) found that the ethyl acetate

extract from the leaves of F. lutea increased insulin response and secretion in obese mouse.

The decoction of F. semicordata bark has been used to treat diabetes in various locations of India (Kaur et al., 2017). Sub

fractions obtained from the ethanol extract of F. semicordata leaves showed a strong antidiabetic activity in streptozotocin-induced

diabetic rats by increasing glucose uptake and decreasing blood glucose level (Kaur et al., 2017). Catechin, rutin, quercetin, dodecane,

Indole, Linalool and germacrene were present in the extract of F. semicordata (Kaur et al., 2016). Another study indicated that
methanol extracts from the bark and leaves of F. infectoria exhibit a potent antidiabetic effect in fructose-induced hyperglycemia rats

by decreasing triglyceride, total cholesterol, LDL, VLDL and serum glucose levels. In addition, the stem bark of F. infectoria contains

methyl ricinolate, caffeic acid, bergenin, β-sitosterol and lanosterol (Gupta et al., 2014). The ethanol extract of F. lyrata leaves

reduced the blood glucose level in alloxan monohydrate-induced diabetic rats (El-Kashoury et al., 2013). In regards to F. ovata,

hydroethanolic extracts from the twigs and fruits significantly reduced fasting blood glucose, triglyceride, total and LDL cholesterol,

creatinine and total protein levels and increased HDL cholesterol and nitric oxide levels in high fructose/high cholesterol diet-induced

diabetic rats (Fouondo et al., 2014). A recent study revealed that F. lacor leaves effectively decreased fasting and postprandial blood

glucose levels in diabetic patients (Sood and Sakshi, 2017).

5. Conclusion

Recently, there is a growing interest in developing natural antidiabetic drugs to manage diabetic complications, especially from

plant sources. Recent studies have reported that the crude extracts and active compounds from various Ficus species exhibit

antidiabetic properties under various in vitro and in vivo models. Particularly, compounds isolated from Ficus species effectively

mitigated all the diabetic-related complications in streptozotocin- and alloxan-induced diabetic animals. Among Ficus species, F.

benghalensis, F. religiosa, F. glumosa, F. deltoidea, F. racemosa and F. carica are the most studied species with strong antidiabetic

potentials. Enhancing insulin sensitivity, inducing insulin secretion, increasing hepatic glycogen synthesis, decreasing carbohydrate

absorption, regulating intestinal tract enzymatic activities, increasing peripheral glucose uptake, and improving antioxidant status are
some important antidiabetic actions of Ficus species. Hence, this review provides a scientific basis for further studies in association

with the development of effective antidiabetic drugs from plant sources, especially Ficus species. Although extracts and active

compounds from different Ficus species possess remarkable antidiabetic activity, mechanisms of antidiabetic action and clinical

studies are insufficient. Hence, further isolation and identification of antidiabetic molecules and evaluation of their mechanisms of

action and clinical studies are required to develop effective antidiabetic drugs from Ficus species.

Acknowledgement

This study was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP;

Ministry of Science, ICT & Future Planning) (No. NRF-2017R1C1B5017445), Korea Institute of Planning and Evaluation for

Technology in Food, Agriculture, Forestry and Fisheries (IPET) through High Value-added Food Technology Development Program,

funded by Ministry of Agriculture, Food and Rural Affairs (MAFRA) (317044-03) and the 2017 Research Grant from Kangwon

National University, Chuncheon, Republic of Korea. The English in this document has been checked by at least two professional

editors, both native speakers of English (American Journal Experts).

Conflict of interests

The authors declare that there is no conflict of interest.


Author’s contributions

P. Deepa and K. Sowndhararajan collected the data and conceptualized the study. P. Deepa, K. Sowndhararajan and S.J. Park

wrote the manicript. S. Kim and K. Sowndhararajan provided helpful comments for the discussion and revised this manuscript. S.J.

Park arranged this manuscript via full communications with all co-authors. All authors read and approved the final manuscript.

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Figure 1. Mechanisms of anti-diabetic action of Ficus species
Figure 2. Some important antidiabetic compounds isolated from Ficus species

69
Figure 3. Maximum dose range used for the antidiabetic effects of bark and leaf extracts
from Ficus species

Bark
1400
Maximum dose range (mg/kg body weight)

1200
1200

1000

800

600 500 500

400
250 240
200 200 200
200 150 150
50
0

Ficus Species

Leaf
1200
Maximum dose range (mg/kg body weight)

1000 1000
1000

800
700

600
500

400 400 400 400 400 400 400 400 400 400
400
300
250 250
200 200 200
200
100
50

Ficus Species

70
Figure 4. Maximum dose range used for the antidiabetic effects of compounds isolated
from Ficus species

Compounds
Maximum dose range (mg/kg body weight)

300
250
250
200
200

150
100 100 100 100 100 100 100 100
100

50
20 15 15

Compounds isolated from Ficus species

71
Table 1. Antidiabetic potential of different Ficus species

S. Plant Part / Dose Experime Positive Dura Activity Referenc


N name extract or nt model control tion e
o. compound

1. F. Bark / 50, Streptozot Glibencl 21 Reduce blood Arunachal


amplissi methanol 100 ocin- amide days glucose, am and
ma Sm. and induced (10 serum Parimelaz
150 mg/kg) triglyceride hagan,
mg/kg diabetic and total 2013
rats cholesterol
levels.

Increase
serum insulin
level.

2. F. Bark / 100 Streptozot Glibencl 21 Decrease Mazumde


arnottia ficanone mg/kg ocin- amide (5 days oxidative r et al.,
na induced mg/kg) stress in 2008
(Miq.) diabetic
Miq. diabetic pancreas and
rats liver. Increase
peripheral
glucose
utilization.

Inhibit
carbohydrate
intake from
intestine and
peripheral
glucose
release.

Increase
insulin
secretion from
the pancreatic
β-cells.

3. F. Stem / 400, Alloxan- - 21 Decrease Omoniwa


asperifo aqueous 800 induced days blood glucose, and Luka,
lia Miq. and diabetic serum 2012
1200 triglyceride

72
mg/kg albino rats and total
cholesterol
levels.

Increase
serum AST
activity.

Bark / 400, Alloxan- - 21 Reduce blood Omoniwa


aqueous 800 induced days glucose, et al.,
and diabetic serum 2014
1200 albino rats triglyceride,
mg/kg total
cholesterol
and LDL
levels.

Increase total
protein
content.

4. F. Bark / 150 - Alloxan- - 30 Decrease Gupta et


benghal aqueous 250 induced days fasting blood al., 2002
ensis L. mg/kg diabetic glucose level
rabbits and enhance
glucose
tolerance.

Root 100, Streptozot Glipizide - Reduce blood Singh et


(elemental 200, ocin - (2.5 glucose level. al., 2009a
Mg and Ca) / 300 induced mg/kg)
aqueous and
400 diabetic
mg kg rats

Root / α- 15, Streptozot Metform - Decrease Singh et


amyrin 25, 50 ocin- in (50 blood glucose al., 2009b
acetate and induced mg /kg) and increase
100 diabetic HDL-C
mg/kg rats Levels.

Leaves / 200 Alloxan- Glibencl 14 Reduce blood Saraswath


ethanol and induced amide days glucose, i et al.,
400 diabetic (5mg/kg) triglycerides 2013
mg/kg rats and
cholesterol
levels.

73
Bark / 100, Streptozot Tolbuta 12 Decrease Gayathri
aqueous 300 ocin- mide week blood glucose and
and induced (100 s level. Kannabira
500 mg/kg) n, 2008
mg/kg diabetic Restore
rats microsomal
protein
concentration
and
cytochrome P-
450 dependent
monooxygena
se enzymes
EROD, PROD
and PNPH.

Reduce the
inflammation
and swelling
in pancreatic
tissue.

Aerial root / 50 Streptozot Metform 10 Decrease Akanksha


α-amyrin mg/kg ocin- in days blood glucose et al.,
acetate induced level. 2010
diabetic
rats

Fruit / 250 Alloxan- Gliclazid 30 Reduce blood Priya et


ethanol mg/kg induced e (5 days glucose and al., 2013.
diabetic mg/kg) total
rats cholesterol
levels.

Bark / 50 Alloxan- - 6 Decrease Shukla et


aqueous mg/kg induced week serum al., 1995
body diabetic s cholesterol,
weigh rabbits low density
t lipoprotein
cholesterol,
triacylglycerol
, glycosylated
haemoglobin
and blood
glucose levels.

Bark / - Glucose- Tolbuta - Control the Bramacha

74
flavonoids induced mide hypoglycemia ri and
(Leucoantho hypoglyca and Augusti,
cyanidia and emic hyperglycemi 1964.
leucoanthocy rabbits a.
anin)/

Bark / - Glucose- Tolbuta - Control the Bramacha


ethanol induced mide hypoglycaemi ri and
hypoglyca (0.5 g) a. Augusti,
emic 1961.
rabbits.

Bark / 250 Alloxan- Glibencl - Reduce blood Geetha


Leucodelphi mg/kg induced amide (2 glucose level. and
nidin diabetic mg/kg). Mathew,
rats 1994.

Bark/ 120 Alloxan- Glibencl 30 Reduce blood Sharma et


Ethanol mg/kg induced amide days glucose level. al., 2007.
diabetic
rats

Bark and 150 Alloxan- Glibencl 28 Reduce blood Chikaradd


Leaves / and induced amide days glucose level. y and
aqueous 300 diabetic (5mg/kg) Maniyar,
mg/kg rats 2017

Bark / hydro 120 Alloxan- Tolbuta 21 Reduce blood Saifi et


alcoholic mg/kg induced mide 100 days glucose and al., 2014
extract diabetic mg/kg serum
rats b.wt cholesterol,
triglycerides,
LDL,
creatinine,
urea, alkaline
phosphatase,
bilirubin,
glutamate
oxalate
transaminase
and glutamate
pyruvate
transaminase
levels.
Increase HDL
and albumin

75
levels.

Bark / 100 Alloxan- - 30 Stimulate Augusti et


leucopelargo mg/kg induced days insulin al., 1994
nidin-3-0- diabetic secretion.
alpha-L dogs
rhamnoside

5. F. Leaves / single Streptozot - - Enhance Perez et


carica chloroform dose ocin- antioxidant al., 2003
L. induced status.
diabetic Normalize
rats fatty acids and
plasma
vitamin E
values.

Leaves / 10 Streptozot Pioglitaz 28 Decrease Irudayaraj


ficusin and20 ocin- one (10 days blood glucose et al.,
mg/kg induced mg/kg) level. 2016
diabetic Improves lipid
rats profile,
plasma
insulin,
nephritic
marker, liver
glycogen,
liver enzymes
and protected
β-cells.

Upregulate
PPARγ and
activates the
glucose
transport
through
translocation
and GLUT4
activation in
adipose tissue.

Leaves / 250 Streptozot Glibencl 28 Decrease Irudayaraj


ethyl acetate and ocin- amide days blood glucose, et al.,
500 induced (0.6 total 2017
mg/kg diabetic mg/kg) cholesterol,
rats triglyceride

76
levels and
body weight.

Enhance
glucose
utilization.

Normalize
glucose-6-
phosphatase,
fructose-1,6-
biphosphatase
and
hexokinase.

Prevent
deterioration
of β-cells.

Leaves / The Streptozot - 3 Enhance Perez et


aqueous leaf ocin- week insulin al.,2000
decoct induced s secretion and
ion diabetic decreases
(2.5 rats plasma
g/100 glucose levels
ml) and improve
was glucose
suppli uptake by the
ed to muscle cells.
rats in
lieu of
drinki
ng
water

Leaves / Decoc Streptozot Insulin - Decrease Perez et


aqueous tion ocin- plasma al., 1996
induced glucose level
diabetic
rats

Fruit and Fed 5, Alloxon- - - Increase El-


Leaves / raw 10 induced antioxidant Shobaki
and diabetic levels. et al.,
20 % rats 2010
for
fruit;
4, 6

77
and 8
% for
leaves

Leaves / 100 Alloxan- Metform 21 Reduce blood Stalin et


methanol and induced in (500 days glucose and al., 2012
200 diabetic mg/kg) triglycerides
mg/kg albino rats levels.

Leaves / 200 Alloxan- Glibencl 20 Decrease Jayakuma


ethanol and induced amide (5 days blood glucose r et al.,
400 diabetic mg/kg) level. 2014
mg/kg rats

Leaves / 13 g Diabetic Insulin 60 Control Serraclara


decoction human days postprandial et al.,
(men and glycemia 1998
women)

Leaves / 0.05, Streptozot - - Decrease Rashidi


aqueous 0.1, ocin- blood glucose and
and induced level. Noureddi
0.4 diabetic ni, 2011.
mg/dl rats

Leaves/ Streptozot - - Decrease total Canal et


decoction ocin- cholesterol al., 2000
induced and
diabetic hyperglycaem
rats ia.

Fruit / 50, Streptozot Metform 14 Reduce blood Sheikh et


methanol 100, ocin- in (500 days glucose level al., 2015
150 induced mg/kg) and increase
mg/kg albino insulin action.
Wister
rats

6. F. cunia Fruit / 50, Streptozot Metform 14 Reduce blood Sheikh et


Ham. methanol 100 ocin- in 500 days glucose al., 2015
Ex. and induced mg/kg concentration.
Roxb. 150 diabetic p.o.
(Syn. F. mg/kg rats
semicor
data)

78
7. F. Leaves / 175, Alloxan- Gliclazid 10 Decrease El-
cyathisti aqueous and 350 induced e (5 days blood glucose Sakhawy
pula ethanol and diabetic mg/kg) level. et al.,
Warb. 700 rats 2016
mg/kg

8. F. Leaves / 100, Alloxan- Glibencl 10 Maintain Ghori et


dalhousi ethanol 200 induced amide days blood glucose al., 2014
ae Miq. and diabetic (10 level, increase
400 rats mg/kg) the level of
mg/kg plasma insulin
and reduce
mortality rate.

9. F. Leaves / 1000 Healthy Insulin 8 Decrease total Kalman et


deltoide aqueous mg adults week and LDL al., 2013
a Jack with pre- s cholesterol
diabetes levels.
(aged 21
to 65)

Leaves / 1, 3 Streptozot Acarbos 14 Reduce blood Choo et


vitexin and and ocin- e days glucose level. al., 2012
isovitexin 15 induced (5 mg/kg
mg/kg )
diabetic
rats

Leaves / 100, Streptozot Metform 14 Reduce blood Ilyanie et


methanol, 200 ocin- in and days glucose al., 2011
aqueous, n- and induced glibencla concentration
hexane, 400 mide and insulin
chloroform mg/kg diabetic (300 and receptor
and n- rats 3 mg/kg) sensitization
butanol effect.

Leaves / 250 Glucose- Metform - Reduce blood Noor et


ethanol and induced in glucose level. al., 2016
500 diabetic
mg/kg rats

Leaves / 250, Streptozot Glibencl 14 Increase Farsi et


petroleum 500 ocin- amide days insulin al., 2014
ether, and induced (10 secretion via
chloroform 1000 mg/kg) down-
and mg/kg diabetic regulation of
phosphoenolp

79
methanol rats yruvate
carboxykinase
and glucose-6-
phosphatase
expressions
and up
regulation of
hepatic GK
and PPARγ
expressions.

Increase
GLUT-4 gene
expression in
skeletal
muscles.

1 F. Leaves / 100 Streptozot - 30 Decrease Adewole


0. exasper aqueous mg/kg ocin- days blood glucose, et al.,
ata Vahl induced blood pressure 2011
Obese and lipid
Zucker profiles.
rats

Leaves / 100, Alloxan- - - Reduce blood Adeyi et


aqueous 200 induced glucose level al., 2012
and diabetic
300 albino rats
mg/kg

Leaves / 250 Fructose- - 21 Normalize Taiwo et


aqueous mg/kg induced days blood glucose al., 2010
diabetic level
rats

Leaves / 100 Streptozot - 8 Reduce blood Adewole


aqueous mg/kg ocin- week glucose level. et al.,
induced s 2012
diabetic
rats

1 F. Fruit / 1, 2, 3 Alloxan- - - Reduce blood Akhtar


1. glomera aqueous and 4 induced glucose level and
ta Roxb. g/kg diabetic and increase Qureshi,
rabbits insulin 1988
secretion.

80
Leaves / 100, Alloxan Glibencl 10 Reduce blood Sharma et
ethanol 250 monohydr amide days glucose, al., 2010
and ate- (10 serum urea,
500 induced mg/kg) creatinine and
mg/kg diabetic cholesterol
rats levels.

Bark / 200 Alloxan- Glibencl 21 Reduce blood Heroor et


methanol mg/kg induced amide days glucose level. al., 2014
diabetic (300 and
rats 600
µg/kg)

1 F. Bark / 62.5, Alloxan- Glibencl - Decrease Madubun


2. glumosa methanol 125, induced amide (2 blood glucose yi et al.,
Delile and diabetic mg/kg) level. 2012
250 mice
mg/kg

Bark / 62.5, alloxan- Glibencl 14 Improve Onoja et


methanol 125, induced amide (2 days glucose al., 2014
and hyperglyc mg/kg utilization and
250 aemic rats antioxidant
mg/kg activities.

Leaves / 100, Alloxan- - 7 Reduce blood Umar et


ethanol 200 induced days glucose level al., 2013.
and diabetic and serum
400 wistar rats lipid profile.
mg/kg

Leaves / 100, Alloxan- Insulin 7 Decrease Usman


ethanol 200 induced days fasting blood and
and diabetic glucose level. Mohamed
400 rats , 2015
mg/kg Increase liver
enzymes
(AST, ALT
and ALP)

1 F. Bark / 6% Alloxan Glibencl - Reduce Ghosh et


3. hispida ethanol (w/v) monohydr amide fasting blood al., 2004
L.f. ate- (0.5 glucose level.
induced mg/kg)
diabetic Increase
rats glycogen
content of the

81
liver, skeletal
and cardiac
muscles.

Leaves / 100, Alloxan- Glibencl 21 Reduce blood Ravichan


methanol 200 induced amide (5 days glucose, dra and
and diabetic mg/kg) serum SGOT, Paarakh,
400 rats triglycerides 2014a
mg/kg and
cholesterol.

Increased
insulin level.

Leaves / 50, Glucose Glibencl - Reduce serum Shahreen


methanol 100, loaded amide glucose level. et al.,
200 mice (10 2012
and mg/kg)
400
mg/kg

1 F. Leaves and 200 Fructose Fenofibr 20 Decrease Gupta et


4. infectori bark/ and induced ate (20 days triglyceride, al., 2014
a Roxb. Methanol 400 hyperglyc mg/kg) total
mg/kg emic rats cholesterol,
LDL, VLDL
and serum
glucose levels.

1 F. Leaves / 200 Alloxan- Glibencl 21 Reduce blood Sidhu and


5. krishnae petroleum mg/kg induced amide days glucose level. Sharma,
C.DC. ether diabetic (2.5 2014.
(Syn. F. rats mg/kg)
benghal
ensis)

1 F. lacor Leaves / - Diabetic - 3 Decrease Sood and


6. Buch.- powder patients week fasting and Sakshi,
Ham. s postprandial 2017.
blood sugar
level.

1 F. lutea Leaves / 42% Obese Glibencl 21 Increase Olaokun


7. Vahl ethyl acetate (w/w) mouse amide days insulin et al.,
fat model response and 2016
and secretion.
36%

82
(w/w)
sugar

1 F. lyrata Leaves / 200 Alloxan Gliclazid 28 Reduce blood El-


8. Warb. ethanol and monohydr e (20 days glucose level. Kashoury
400 ate- mg/kg) et al.,
mg/kg induced 2013
diabetic
rats

1 F. Leaves / 100, Alloxan- Glibencl 21 Reduce blood Ravichan


9. microca methanol 200 induced amide days glucose, dra and
rpa L.f. and diabetic (5mg/kg) cholesterol Paarakh,
400 rats and 2013
mg/kg triglycerides
levels.

Increase
insulin level.

Leaves / 100 Alloxan- Glibencl 15 Increase HDL Kumar et


ethanol and induced amide days and al., 2007
200 diabetic (5mg/kg) antioxidant
mg/kg rats enzyme levels
and reduce
blood glucose,
triglycerides,
total
cholesterol,
LDL and
VLDL levels.

Leaves / 200 Alloxan- Glibencl 14 Reduce serum Lakshmi


petroleum and induced amide days glucose, total et al.,
ether 400 diabetic (2.5mg/k cholesterol, 2010.
mg/kg rats g) LDL, VLDL
and
triglycerides
levels.

2 F. Leaves / 200 Dexameth Glibencl 10 Reduce blood Munna


0. mollis ethyl acetate and asone- amide days glucose level. and
Vahl 400 induced (500 Saleem,
mg/kg diabetic µg/mg) 2013
rats

Leaves / 100, Alloxan- Glibencl 21 Reduce blood Ravichan

83
methanol 200 induced amide days glucose level, dra and
and diabetic (5mg/kg) concentration Paarakh,
400 rats of SGOT, 2014b
mg/kg triglycerides,
cholesterol
and urea.

2 F. Leaves / 250 Alloxan- Glibencl 10 Reduce blood Devi et


1. nervosa ethanol and mg/kg induced amide days glucose, al., 2012
B.Heyne ethyl acetate diabetic (10 serum urea,
ex Roth rats mg/kg) creatinine and
cholesterol
levels.
Increase
protein level.

Leaves / 200 Streptozot Glibencl 14 Reduce serum Raj et al.,


petroleum and ocin- amide days glucose, total 2011
ether 400 induced (600 cholesterol
µg/kg) and
mg/kg diabetic
triglycerides.
rats

2 F. Leaves / 50 Streptozot Glyburid 14 Restore blood Degollado


2. odorata dichlorometh and ocin - e (10 days glucose level et al.,
(Blanco) ane 200 induced mg/kg) near to 2014
Merr. mg/kg diabetic normal.
rats

2 Ficus Twigs and 300 Fructose/ - - Reduce Fouondo


3. ovata fruit / mg/kg high fasting blood et al.,
Vahl hydroethanol cholestero glucose, 2014
ic extract l diet- triglyceride,
induced total and LDL
diabetic cholesterol,
rats creatinine and
total protein
levels.
Increase HDL
cholesterol
and nitric
oxide levels.

2 F. Leaves / 50, Streptozot Glibencl 21 Reduce blood Singh et


4. palmata hydroalcohol 100 ocin- amide days glucose, al., 2014.
Forssk. ic extract and induced (10 mg serum
200 diabetic kg) triglyceride
and total

84
mg/kg rats cholesterol
levels.

Increase
serum insulin,
body weight
and glycogen
content in
liver and
skeletal
muscle.

2 F. Leaves / 200 Alloxan- Gliclazid 28 Reduce blood El-


5. platypod ethanol and induced e (20 days glucose level. Kashoury
a (Miq.) 400 diabetic mg/kg) et al.,
A.Cunn. mg/kg rats 2013
ex Miq.

2 F. Leaves / hot 100, Glucose, Acarbos - Decrease Salonga et


6. pseudop water extract 500 maltose e (5 blood glucose al., 2013
alma and and starch mg/kg), level.
Blanco 1000 loaded Glibencl
mg/kg mice amide (3
mg/kg)
and
Metform
in (250
mg/kg).

2 F. Leaves / 200 Streptozot Glibencl 21 Decrease Thamotha


7. pumila ethanol and ocin- amide days blood glucose, ran et al.,
L. 400 induced (10mg/k LDL, VLDL, 2013
mg/ diabetic g) TC and TG
kg rats levels.

Increase HDL
level.

Fruit / pectic 100 C57BL/K Rosiglita - Activate Wu et al.,


polysacchari and sJ db/db zone (2 1/phosphatidy 2017
de 200 mice mg/kg) linositol-3
mg/kg kinase /protein
kinase
B/glycogen
synthase
kinase-3β.

Regulate

85
glucokinase,
phosphoenolp
yruvate
carboxykinase
and glucose-6-
phosphatase.

2 F. Bark/ 200 Streptozot - 8 Antioxidant Joshi et


8. racemos ethanol and ocin- week activity. al., 2016
a L. 400 induced s
mg/kg diabetic Restore blood
rats glucose and
lipid levels.

Reduce the
creatinine
kinase, blood
urea nitrogen,
collagen and
albumin
levels.

Root / 100, Streptozot Glibencl 15 Reduce blood Varma et


methanol 200 ocin- amide days glucose level. al., 2009
and induced 500
400 diabetic (µg/kg)
mg/kg rats

Bark/ 4 100 Streptozot Glibencl 7 Reduce blood Keshari et


isolated mg/kg ocin- amide days glucose level al., 2016
flavonoids induced (10 and restore
(similar to diabetic mg/kg) body weight.
kaemferol, rats
quercetin, Express
naringenin hypoglycemic
and action via
baicalein) binding to
PPARγ and
GLUTI
receptors.

Leaves / 100 Streptozot Glibencl 7 Reduce blood Kushwaha


sterols mg/kg ocin- amide days glucose level et al.,
induced (10 and serum 2015
diabetic mg/kg) lipid
rats parameters.

Improved

86
HDL level
and restore
body weight.

Bark / 100 Hypoglyc Sulfonyl 15 Reduce blood Gul-E-


aqueous mg emia in urea days glucose level. Rana et
humans al., 2013
with
diabetes

Bark / 100 Streptozot Metform 30 Reverse the Ravichan


acetone and ocin- in days increased diran et
(tannin 200 induced blood glucose, al., 2012
fraction) mg/kg diabetic total
. rats cholesterol,
triglycerides
and LDL
levels.

Restore
insulin and
HDL levels in
the serum.

Restore
antioxidant
status of the
organs to
normal levels.

Fruit / 1.25 Streptozot - - Enhance Jahan et


aqueous g/kg ocin- disposal of al., 2009
ethanol induced glucose by
(80%) diabetic increasing
rats insulin
sensitivity.

Bark / 300 Alloxan- Glibencl 45 Restore blood Sophia


ethanol mg/kg induced amide days glucose, lipids and
diabetic (600 and Manohara
rats µg/kg) lipoprotein n, 2007
levels to near
normal range.

Bark / 200 Alloxan- Glibencl - Reduce blood Bhaskara


and induced amide Rao et al.,

87
methanol 400 diabetic (10 glucose level. 2002
mg/kg rats mg/kg)

Bark / tannin 100 Streptozot Metform 30 Reverse the Velayutha


and ocin- in days increased m et al.,
200 induced blood glucose, 2012
mg/kg diabetic total
rats cholesterol,
triglycerides,
LDL levels.

Restore
insulin and
HDL levels in
the serum.

Leaves / 100, Alloxan- Glibencl 2 Reduce blood Patil et


ethanol 200 induced amide week glucose level al., 2010
and diabetic (10 s
300 rats mg/kg)
mg/kg

Leaves / 100, Streptozot Glibencl 7 Reduce blood Yadav et


petroleum 200 ocin- amide days glucose level, al., 2015
ether and induced (10 serum
300 diabetic mg/kg) cholesterol,
mg/kg rats triglycerides,
LDL and
VLDL.

Improve HDL
level.

Restore body
weight.

Increase
glutathione,
catalase and
superoxide
dismutase.

Fruit / 100, Alloxan- Glyburid 21 Enhance Deshmuk


petroleum 200 induced e (10 days glucose h et al.,
ether and diabetic mg/kg) utilization. 2007
400 mice
mg/kg Reduce serum
glucose level.

88
Seed / 200 Streptozot Metform - Decrease Urmi et
aqueous mg/kg ocin- in (500 blood glucose, al., 2012
induced µg/ kg) triglycerides,
diabetic total
rats cholesterol
and LDL.

Bark / 200 High fat Pioglitaz - Reduce blood Veerapur


ethanol and diet and one (10 glucose level et al.,
400 low dose mg/ kg) and increase 2012
mg/kg streptozot serum insulin
ocin- level.
induced
diabetic
rats

Fruit / 100 Alloxan- Metform 14 Restore blood Zulfiker


Ethanol and induced in days glucose level. et al.,
200 Swiss hydrochl 2011
mg/kg albino oride
mice 600
(µg/kg)

Root bark / 250 Alloxan- Tolbuta 1 Decrease Goyal and


ethanol mg/kg induced mide week blood sugar Jain,
diabetic (250 level. 2012.
rabbits mg/kg)

Bark / 250 Streptozot Glibencl 28 Reduce blood Solanki


methanol and ocin- amide days glucose level. and
and aqueous 500 induced (2.5 Bhavsar,
mg/kg diabetic mg/kg) 2015.
wistar
rats.

Bark / 400 Alloxan- Tobutam 1 Reduce blood Sachan et


ethanol and mg/kg induced ide (100 week glucose level. al., 2009.
aqueous diabetic mg/kg)
rats

2 F. Bark / 100 Streptozot Gliclazid 4 Decrease the Kirana et


9. religios aqueous and ocin- e (10 week elevated al., 2011
a L. 200 induced mg/kg) s glucose and
mg/kg neonatal TNF-α.
rat model

89
Bark / 25, 50 Streptozot Glibencl 21 Reduce blood Pandit et
aqueous and ocin- amide days glucose and al., 2010
100 induced (10 serum
mg/kg mg/kg). triglyceride
diabetic and total
rats cholesterol
levels.

Increase
serum insulin,
body weight
and glycogen
content in
liver and
skeletal
muscle.

Leaves / 250 Alloxan- Tolbuta 21 Decrease Pochhi


aqueous mg/kg induced mide days blood glucose, and
diabetic serum Muddesh
rats cholesterol war, 2017
and
triglyceride
levels.

Stem bark / - Streptozot - - Reduce blood Priyanka


Nanoparticle ocin- glucose level. et al.,
s induced 2018
diabetic
rats

Powder 100, Streptozot - 4 Reduce Rathi et


200 ocin- week fasting plasma al., 2016
and induced s glucose level,
400 diabetic body weight
mg/kg rats and plasma
tumor necrosis
factor-α level.

Leaves and 100 Alloxan- Glibencl 30 Decrease Goswami


fruit / and induced amide days blood glucose et al.,
ethanol 250 diabetic (600 level by 2010
mg/kg rats µg/kg) stimulating β-
cells to release
insulin.

3 F. Leaves / 50 Streptozot Glibencl 21 Increase Kaur et

90
0. semicor ethanol (Sub mg/kg ocin- amide days glucose al., 2017
data fractions) induced (30 uptake and
Buch.- diabetic mg/kg) decrease
Ham.ex rats blood glucose
sm. level.

3 F. Bark / 50, Alloxan- Insulin 30 Reduce blood Njagi et


1. sycomor aqueous 100 induced days glucose level. al., 2012
us L. and diabetic
150 mice
mg/kg

3 F. Bark / 100 Streptozot Glibencl 21 Increase Arunachal


2. talbotii methanol and ocin- amide days serum insulin, am, and
King 200 induced (10 HDL and Parimelaz
mg/ diabetic mg/kg) plasma hagan,
kg rats enzymes and 2014
glycogen level
in the liver
and muscle.

Decrease
fasting blood
glucose and
serum marker
enzymes
levels.

Decrease total
cholesterol
and serum
triglycerides
levels.

3 F. Bark / 60, Streptozot Metform 5 Decrease Musabaya


3. thonnin ethanol 120 ocin- in week blood glucose ne et al.,
gii and induced s level. 2007
Blume 240
mg/kg diabetic
rats

91
Table 2. Antidiabetic uses of different Ficus species in traditional medicine and their
bioactive components.

S. Species Bioactive Part Mode of utilization Area of References


N name compounds used tradition
o. al use

Arunachala
1. F. γ-Sitosterol, lup- Bark Suravappidippaanundai Sri
m and
amplissim 20(29)-en-3-yl Lankan
Parimelazha
a Sm. acetate, lupeol, Siddha
gan, 2013;
myristic acid, Medicine
Sathasivamp
ergost-5-en-3-ol, β-
illai et al.,
stigmasterol,
2017;
stearic acid, phytol,
Murugan et
sitosterol and
al., 2012
lanosterol acetate
Mazumder
2. F. Ficanone, Sterols, Bark - Local
et al., 2008;
arnottiana alkaloids, inhabitan
Jayachandra
(Miq.) carbohydrates, ts of
n and
Miq. tannins and Tamil
Mahesh,
phenolic Nadu
2007;
compounds
Babu et al.,
2017
3. F. Alkaloids, Leav - Igala Gbolade,
asperifolia flavonoids, es tribe of 2009;
Miq. glycosides, resins, Logas Omoniwa
saponins, tannins, and Kogi and Luka,
terpenes, steroids state, 2012;
and phenolic Nigeria Omoniwa et
compounds. al., 2014;
Momoh et
al., 2017
4. F. Betulinic acid, Fruit, Extract Tribes of El-Fishawy
auriculata lupeol, bark Wayanad et al., 2011;
Lour. stigmasterol and β- and District, Raghavendr
sitosterol-3-O-β-D- root Kerala, a et al., 2015
glucoside India
5. F. Mg, Ca, Stem Extract and raw part Pakistan Singh et al.,
benghalen leucopelargonin , bark, 2009a;
sis L. α-amyrin acetate, fruit Khan et al.,
leucopelargonidin- and 2011
3-0-alpha-L fresh
rhamnoside, prop
sterols, ketones, root
flavonoids, tips
triterpenes,
Leaf Mature raw part Rural Gayathri and
furocoumarins and
and Kannabiran,
tiglic acid esters
urban 2008;
areas of Ocvirk et al.,
Dhaka, 2013

92
Banglade
sh
Leav Decoction Udhamp Singh et al.,
es, ur, 2009b;
stem Jammu Bhatia et al.,
and and 2014
bark Kashmir,
India
Bark Suravappidippaanundai, Sri Augusti et
and Piramehakkulihai and Lankan al., 1994;
root Kudineer Siddha Sathasivamp
Medicine illai et al.,
2017
Arshad et
Milk Eaten raw Chitta
al., 2014;
y hills of
Mandal et
latex Pothwar
al., 2010
region,
Pakistan
Bark - Local Jayachandra
inhabitan n and
ts of Mahesh,
Tamil 2007
Nadu
6. F. carica Phenolics, Root Boiled root Bapedi El-Shobaki
L. flavonoids, ficusin, healers et al., 2010;
triterpenoids, in Semenya et
steroids, Limpopo al., 2012
coumarins, Province,
flavones, Psoralen, South
bergapten, Africa
quercetin 3-O-
Fruit Powder Errachidi Jayakumar
rutinoside, ferulic
and a, South et al., 2014;
acid, 3-O
leave eastern Tahraoui et
caffeoylquinic acid
s Morocco al., 2007
and 5-O-
caffeoylquinic Leav Decoction Pakistan Mopuri and
acid. es Islam, 2016;
Khan et al.,
2011;
Mahmoudi
et al., 2016
Fruit Decoction Chtouka Irudayaraj et
Ait Baha al., 2016;
and Barkaoui et
Tiznit, al., 2017;
Morocco Jain et al.,
2013
7. F. cunia - Fruit Eaten raw Northeas Sheikh et al.,
Ham. Ex. t India 2015
Roxb.
(Syn. F.

93
semicorda
ta)
8. F. α-Amyrin, lupeol - - - El-Sakhawy
cyathistip acetate, taraxerol, et al., 2016
ula Warb. β-sitosterol,
protocatechuic acid
and 3-O-caffeoyl
quinic acid
9. F. Flavonoids - - - Ghori et al.,
dalhousia 2014
e Miq.
10 F. Flavonoids , Leav Eaten raw Singapor Adam et al.,
. deltoidea flavone C- es e 2012; Farsi
Jack glycosides, vitexin et al., 2014;
and isovitexin Choo et al.,
2012; Siew
et al., 2014
11 F. Coumarins, Root Decoction South Adewole et
. exasperat flavonoids, Western al., 2011;
a Vaghl saponins, Nigeria Abo et al.,
alkaloids, tannins 2008
and cyanogenic
Leav Decoction Nigeria Ezuruike
glycosides
es, and Prieto,
root, 2014; Ijeh
fruits and Agbor,
and 2006
latex
Leaf, Maceration and Hausa– Yakubu et
root decoction Fulani al., 2014;
and tribes in Shinkaf et
bark Sokoto, al., 2015
Northwe
st
Nigeria
Leav Decoction Kisangan Katemo et
es i, Congo al., 2012
12 F. Flavonoids, - - Sharma et
. glomerata tannins, β- al., 2010;
Roxb. sitosterol, Rumzhum et
leucocyanidin-3-O- al., 2012
β-D-
glucopyrancoside,
leucopelargonidin-
3-O-β-D-
glucopyranoside,
leucopelargonidin-
3-O-α-L-
rhamnopyranoside,
lupeol, ceryl
behenate, lupeol
acetate, α-amyrin

94
acetate,
leucoanthocyanidin
and
leucoanthocyanin,
stigmasterol,
Glauanol acetate
and racemosic acid
13 F. Tannin, saponins, Leav - Africa Olaokun et
. glumosa alkaloids, es, al., 2013
Delile glycosides, stem
flavonoids and and
triterpenes bark
Bark - Enugu Madubunyi
State, et al., 2012;
Nigeria Ntchapda et
al., 2014
14 F. hispida Glycosides, Fruit Raw ripe fruit Sugali Basha et al.,
. L.f. hispiloscine, tribal 2011;
ficushispimines A inhabitan Howlader et
and B, C, ??-amyrin ts of al., 2017
acetate, N- Yerramal
triacontanyl ais of
acetate, lupeol Kurnool
acetate, and 10- district,
ketotetracosyl Andhra
arachidate Pradesh,
India
Sap Extract rural Ghosh et al.,
from communi 2004; Tarak
the ty of et al., 2011
root Dhemaji
district
of
Assam,
Northeas
t India
Fruit Eaten raw Santal Rahmatullah
tribe in et al., 2010a
Rangpur
district,
Banglade
sh
Leaf - Kavirajes Rahmatullah
and of et al., 2010b
seed Chalna
area,
Khulna
district,
Banglade
sh
Bark Infusion Pakistan Khan et al.,

95
2011
15 F. Zn, Mg and Mn - - - Sidhu and
. krishnae Sharma,
C.DC. 2014

(Syn. F.
benghalen
sis)
16 F. lacor - Fruit Powder Pakistan Khan et al.,
. Buch.- 2011
Ham.
17 F. lutea Epiafzelechin, - - - Olaokun et
. Vahl catechins and al., 2016
epicatechins
18 F. lyrata Glycosides, - - - El-Kashoury
. Warb. tannins, et al., 2013
flavonoids, sterols
and triterpenes
19 F. polyphenols, Fruit Raw part Pakistan Khan et al.,
. microcarp organic acids, and 2011; Jiang
a L.f. alkaloids, leave et al., 2014;
polysaccharides, s Chan et al.,
Megastigmanes, 2017
pheophytins,
Bark - Tamil Jayachandra
catechin,
and Nadu, n and
epicatechin and
leave India Mahesh,
isovitexin
s 2007
20 F. mollis Flavonoids - - - Munna and
. Vahl Saleem,
2013
21 F. nervosa Flavonoids, Whol - Tirupathi Devi et al.,
. B.Heyne terpenoids, 3- e , India 2012; Chen
ex Roth Hydroxyxanthyleti plant et al., 2010
n, 3-
methoxyxanthyleti
n, xanthyletin,
umbelliferone,
scopoletin and (þ)-
(S)-marmesin
22 F. odorata Flavonoids - - - Degollado et
. (Blanco) al., 2014
Merr.

23 F. Psoralene, trans- Fruit Eaten raw Kala Arshad et


. palmata psoralenoside, Chitta al., 2014;
Forrssk. germanicol acetate, hills of Alqasoumi
bergapten, vanillic Pothwar et al., 2014;
acid, rutin, gallic region, Singh et al.,
acid, ellagic acid, Pakistan 2014

96
β-sitosterol,
sigmasterol,
glaunol acetate,
ceryl behenate,
lupeol, α-amyrin
and β-amryin
acetate
24 F. - Fruit Decoction Hausa– Shinkaf et
. platyphyll Fulani al., 2015;
a Delile tribes in
Sokoto,
Northwe
st
Nigeria
25 F. Glycosides, - - - El-Kashoury
. platypoda tannins, et al., 2013;
(Miq.) flavonoids, sterols, Afifi et al.,
A.Cunn. triterpenes, 3- 2014
ex Miq. Methoxycarpachro
mene,
pheophorbide-a
methyl ester,
pheophorbide-b
methyl ester, 3-
oxo-6-hydroxy-α-
ionol, β-sitosterol-
3-O-β-D-
glucopyranoside
and rutin
26 F. Berberine, Leav Decoction Bicol Salonga et
. pseudopal squalene, es region, al., 2013;
ma polyprenol, β- Philippin Llagas et al.,
Blanco amyrin fatty acid es 2014
ester, α-amyrin
acetate, β-amyrin
acetate, lupeol fatty
acid ester,
lupenone, oleane,
and ursenone
27 F. pumila Phenolics, Leav - Okinawa Thamothara
. L. apigenin, luteolin, es n elders, n et al.,
rutin, genistein, Japan 2013;
hesperidin, Mitsuhashi,
astragalin, 1988;
isoquercitrin, Ashraf et al.,
chrysin, 2013
glycosides, sterols
and triterpenes
28 F. Phenolics, Root Decoction Chana Ravichandir
. racemosa flavonoids, and an et al.,
L tannins, saponins Nathawe 2012;
and alkaloids, e district, Neamsuvan

97
vitamin E and C, Songkhla et al., 2015
β-carotene, β- Province,
Sitosterol, Thailand
stigmasterol,
Fruit Juice Sikkim Zulfiker et
lanosterol,
and al., 2011;
leucocyanidin-3-O-
Darjeelin Chhetri et
β-D-
g al., 2005
glucopyranoside,
Himalay
leucopelargonidin-
an tribes,
3-O-β-D-
India
glucopyranoside,
leucopelargonidin- Bark Mature and premature Rural Patil et al.,
3-O-α-L- and raw part and 2010;
rhamnopyranoside, fruit urban Ocvirk et al.,
cycloartenol, areas of 2013
euphorbol and its Dhaka,
hexacosanoate, Banglade
taraxerone, sh
tinyatoxin, Fruits Raw ripen fruits Santal Kushwaha et
Glauanol, Tribe of al., 2015;
hentriacontane, Joypurha Mahbubur
glauanolacetate, t District, Rahman,
esters of Banglade 2015
taraxasterol, sh
lupeolacetate,
friedelin, and other Bark Periya kulihai, Sri Ahmed and
phytosterols and Ayakkaanthakkulihai, Lankan Urooj, 2009;
latex Suravappidippaanundai, Siddha Sathasivamp
Naaval ney, Medicine illai et al.,
Vachchirasinthaamani 2017; Murti
irasaayanam, and Kumar,
Piramehachchanthanaath 2012
iyennai and Kudineer
Fruit Eaten raw Goro Keshari et
hills of al., 2016;
Durgapur Kushwaha et
, al., 2015;
Banglade Khan et al.,
sh 2015
Root Eaten raw Javadhu Thirumalai
hills, et al., 2012;
Tamil Yadav et al.,
Nadu, 2015
India
Bark - Local Varma et al.,
and inhabitan 2009;
root ts of Jayachandra
Tamil n and
Nadu Mahesh,
2007
Stem Decoction Pakistan Velayutham
bark et al., 2012;
and Khan et al.,

98
ripe 2011
fruit

Flavonoids,
29 F. Bark Hot water extract Pakistan Pandit et al.,
coumarins,
. religiosa 2010; Khan
phenolic acids,
L. et al., 2011
flavonoids,
tannins, lupeol, β- Leav - Africa Kirana et al.,
sitosterol, β- es, 2011;
sitosterol-d- bark Olaokun et
glucoside, and al., 2013
stigmasterol, stem
lanosterol, Bark Suravappidippaanundai Sri Kirana et al.,
campesterol, Lankan 2009;
octacosanol, Siddha Sathasivamp
methyl oleonate Medicine illai et al.,
and lupen-3- one. 2017;
Priyanka et
al., 2017
30 F. Catechin, rutin, Bark Decoction Assam, Kaur et al.,
. semicorda quercetin, Arunach 2017
ta Buch.- dodecane, Indole, al
Ham.ex Linalool and Pradesh,
sm. germacrene Manipur,
Mizoram
, Tripura,
and
Nagaland
of India
31 F. Tannins, saponins, Stem - Africa Njagi et al.,
. sycomorus flavones, bark, 2012;
L. aglycones, leave Olaokun et
anthraquinone s and al., 2013;
glycosides and root Al-matani et
flavonoid al., 2015;
glycosides Bekheet et
al., 2011
32 F. talbotii Rutin, quercetin Aeria - - Arunachala
. King and kaemfeorl l m, and
parts Parimelazha
/ gan, 2014
India
33 F. Anthraquinones, Leav Decoction Nigeria Ezuruike
. thonningii glycosides, es, and and Prieto,
Blume flavonioids, stem Africa 2014;
alkaloids steroids, bark Olaokun et
aglycones, tannins, and al., 2013;
triterpenes and Khan et al.,
fruits
saponins 2011; Ahur
et al., 2013;
Maiha et al.,
2013

99
34 F. virens - Leav Raw Pakistan Khan et al.,
. Aiton es 2011

100

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