Journal o~~thno~har~aeo~ogy, 14 (1985) 173-185 173

Elsevier Scientific Publishers Ireland Ltd.

CHEMISTRY AND PHARMACOLOGY OF AN ETH~OL EXTRACT OF

BUMEL~A SARTORUM~

REINALDO NOBREGA ALMEIDA, JOSE MARIA BARBOSA FILHO and

SURESH RAMNATH NAIK**
~rnivers~dade Federal da Paraiba, Laboratario de ~echnolgia ~ar~aceutica, Cidade
Universitaria, 58.000 Joao Pessoa, Paraiba (Srazil)
(Accepted July 24, 1985)

Summary

Bumelia sartorum has been mentioned in Brazilian folklore for its re-
puted use in the treatment of diabetes mellitus and inflammatory disorders.
An ethanol extract of root bark elicited a hypoglycemic effect in normal
and alloxan-induced diabetic rats. In addition, the extract altered glucose
tolerance in allox~-induced diabetic rats, enhanced glucose uptake in
skeletal muscle and significantly ~hibited glycogenolysis in the liver.
These results indicate that the hypoglycemic effect may be similar to chlor-
propamide and possibly due to an enhanced secretion of insulin from the
islets of Langerhans or an increased utilization of glucose by peripheral
tissues. Besides hypoglycemic activity, the ethanol extract also elicited
signific~t anti-in~ammato~ activity, but did not show any significant
effects on blood pressure, respiration or on the various isolated tissue pre-
parations studied. Bassic acid has been isolated from the ethanol extract
and this component may be responsible for the observed anti-inflammatory
activity. However, it is yet to be established whether bassic acid is respon-
sible for the observed hypoglycemic activity of the ethanol extract,

Introduction

Bumelia sartorum Mart is a large and tall (lo--15 m) tree from the Sapo-
taceae family popularly known as “Quixaba”, “Quixabeira”, “trance-
porteira “, “Sacutiaba” and “rompe-gibao” in northeastern Brazil. Its natural
geographic habitation stretches from north of Minas Gerias to Piaui.

*Part of the work has been submitted to the Federal University of Paraiba, Joao Pessoa,
Brazil, in partial fulfillment of RNA’S M.Sc. degree in Chemistry and Pharmacology
of Nat.ural Products.
**Present address for correspondence: Pharmacology and Toxicology Section, Research
Centre, Hindustan Antibiotics Limited, Pimpri, Pune 411-018, India.

03788741/85/$04.90 01985 Elsevier Scientific Publishers Ireland Ltd.

Published and Printed in Ireland
174

Root bark of this plant has long been used in Brazilian folklore for the
treatment of diabetes mellitus and inflammatory disorders. Systematic
phytochemical studies in the Chemistry Section of this University have
revealed the presence of large quantities of triterpenoids and steroids. So
far, there is no scientific literature correlating ethnobotanical data with
ethnomedical data.
This paper reports the pharmacological effects of an ethanolic extract
of root bark of B. sartorum in laboratory animals and the isolation and
identification of a compound (2/3,3p,4a)-2,3-23-trihydroxyoleana-5,12-
dien-28-oic acid, or bassic acid, from this extract.

Experimental

Chemistry, isolation and identification

The isolation procedure is summarized in the flow-sheet diagram of

Fig. 1.
B. sartorum was collected from Campina Grande, a place in Paraiba
State during the period of October to December. The herbarium sheets
were prepared and deposited with the Botany Section of our laboratory.

PULVERISED ROOT BARK DF BUMELIA SARTDRUMMART

I
Extract in soxhlet w:th hexane fdr 16 hrs.

HEXANE EXTRACT

Rejected a) Concentration with rotary vaccum evaporator.

b) Hydrolysis with 10% ii2SO~ for 2 hrs
c) Filtration in Buchner

Extraction in soxhlet
with CHCL3 for 15 hrs

CHLOf?DFDFW EXTRACT 1
I
a)

E4
Concentration in rotary vaccum evaporator
b) Chromatographic separation on silica gel column using initially
Benzene: Chloroform and thereafter, Chlcroform : Methanol,

BASSIC ACID

Fig. 1. Scheme for the preparation of the ethanol extract of B. snrtorum and the iso-
lation of bassic acid.
 175

The plant materials were processed after obtaining an authentication report

from the Botany Section.
Acid hydrolysis of the 95% ethanol extract from the root bark of the
talus of B. sartorum previously defatted with hexane yielded compound
(I): m.p. 290~-292°C; C,,,HEO,; m/e 486 (&I+); presented a positive Lieber-
mannBuchard reaction; urn!; 3430 Broad, (OH), 1690 (COOH) and 820
(C=C) cm-l. Treatment of compound I with diazomethane yielded a methyl
ester (Ia), m.p. 217.-218°C; C3iH4s05; m/e 500 (M+); ~2% 3430 (OH),
1710, 1725 (COOCHJ) and 855 (C=C) cm-‘. Acetylation of Ia with acetic
anhydride and pyridine produced a triacetate ester (Ib), m.p. 144-146°C;
C3JI5408; m/e 626 (M+); Urna KBr 1740 and 1735 Broad (COOCH3) and 820
(C=C) cm -‘. The NMR spectrum data are summarized in Table 1.
Under the electronic impact in mass spectrometry, the C ring in com-
pound I splits presenting a typical fragmentation which is related to a
retro Diels-Alder reaction (Budzikiewicz et al., 1963). This results in two

TABLE 1

DATA OF NMR SPECTRA WITH CDCl, (VALUES IN 6 )

I : R1,$=R3,Rb,H
(basic acid)
Ia : R1=R2=R3=H., RI=1343
Ib : Rl=R2=Rhc., RL=CH3

0.91 (s, 6H); 0.95, 0.92, 0.94, 1.04,

---C-C& 1.06, 1.27, 1.41 1.25, 1.32, 1.62
(s, each, 12H) (s, each, 18H)
3.64 (s, 3H) 3.64 (s, 3H)
3.70 (m, 1H)
4.20 (m, 1H)
3.65 (m, 2H)
5.55 (m, 1H) 5.58 (m, 1H)
5.42 (m, 1H) 5.44 (m, 1H)
2.92 (dd, 1H) 2.92 (dd, 1H)
- 1.99, 2.05, 2.09
(s, each, 9H)
C&--OAC - 5.02 (d, lH, J = 4 Hz)
Cq$-OAC - 5.41 (m, 1H)
Cg,)B,--CAC 4.00 (ABq, 2H, J = 12 Hz)

Abbreviations: s = singlet, d = doublet, m = multiplet, ABq = AB type quartet.

176

fragments, the most stable of which is the diene fragment (a) which contains
rings D and E.
Ion a is subjected to a new fragmentation where the carbomethoxy
portion is lost to give the more stable fragment (b), the base peak being
due to decreased tension at that point. The other portion of the molecule
from the A and B rings represents fragment (c) (see Fig. 2).
Although bassic acid has been characterized as a common sapogenol
in Sapotaceae (Haywood and Kon, 1940; Simonsen and Ross, 1957;
Varshney and Badhwar, 1971), it is isolated here for the first time from the
genus Bumelia. The mass spectral fragmentation, together with the NMR
and IR spectra of the natural compound and its derivatives (King and
Yardley, 1961; Kitagawa et al., 1972; Banerji et al., 1978), provides strong
evidence that the sapogenol presented here is identical to the bassic acid
reported in the literature.

Pharmacological studies

Wistar strain albino rats weighing 150 200 g and Swiss strain albino
mice weighing 25 --30 g were used. Animals were housed at a constant
temperature of 24°C and allowed free access to food and water. Testing
was carried out during the light portion of 12-h light/dark cycles. Various
other animals, guinea pigs, rabbits and frogs were also used as specified.

Acute toxicity and general pharmacological screening

Acute toxicity was determined in mice and rats by employing various

1’

m/e 203 (100%)

M’ 500 (3%)

m /e 238 (53’10)

Fig. 2. Fragmentation from high resolution electron impact mass spectroscopy.

 177

logarithmic dosages via intraperitoneal and oral routes and observed for
behavioral alterations and mortality during the 72 h following treatment.
The effect of the ethanol extract of B. sartorum (EE) as prepared in Fig.
1 (yield = 32%) was investigated on blood pressure, respiration and cardiac,
skeletal and smooth muscles in experimental animals using both in vivo
and in vitro techniques. Since the toxicity of EE by the oral route was very
low, this route was used for all subsequent experimental studies.
Anti-inflammatory activity was assessed by the carrageenan hind-paw
edema test of Winter et al. (1962). Edema was induced by injecting 0.1 ml
of 1% (w/v) calcium carrageenan (Marine Colloids Inc., Springfield, NJ
07081, U.S.A.) prepared in normal saline and injected subcutaneously
into the plantar region of the left hind-paw. Extract or drug was admini-
stered orally 1 h prior to carrageenan injection. Paw edema was measured
by plethysmographic methods just before and 3 h after carrageenan injec-
tion. The ED5,, of extract for edema inhibition was calculated. Analgesic
activity of EE was estimated using the tail clip (Bianchi and Franceschini,
1954) and acetic acid-induced writhing (Witkin et al., 1961) methods.
Anticonvulsant activity was evaluated in mice using the pentylenetetrazol
seizure test described by Swinyard et al. (1952).

Hypoglycemic activity screening

In normal rats and rabbits

Fasting blood glucose (FBG) of rats (overnight fasted) and rabbits (fasted
for 36 h) was determined using the method of Copper and Mendaniel
(1970). Animals were randomly divided into different groups receiving
EE at various appropriate oral doses. Blood was collected at specific time
intervals by cardiac puncture (rats) or ear vein puncture (rabbits) for glucose
determination.

Epinephrine-induced hyperglycemia in rats

Rats weighing 150~-200 g were randomly divided into three groups of
10 each after determining their FBG levels. Two groups received either
EE (1000 mg/kg) or chlorpropamide (100 mg/kg) while the other received
only 0.9% saline (10 ml/kg) orally. Epinephrine hydrochloride (0.8 mg/kg)
was administered intraperitoneally to all the animals 2 h after the extract
treatment. Blood glucose was determined 30 min and 60 min after epine-
phrine treatment.

Alloxan-induced diabetes in rats

A group of 40 rats were administered alloxan monohydrate (Sigma
Chemicals, U.S.A.) subcutaneously (s.c.) at a dose of 150 mg/kg. FBG
was determined in each rat prior to alloxan administration. Blood glucose
was determined on the 5th day after alloxan administration. Animals show-
ing high blood glucose levels (>200 mg%) were selected and randomly
178

divided into three groups, each containing 10 rats. One group received
extract (500 mg/kg per day p.o.) while the second group received chlor-
propamide (50 mg/kg per day p.o.) for 12 days from day 5 to day 16. The
remaining group served as control and received 0.9% saline (10 ml/kg
per day p.o.) only. Blood samples were collected on days 9, 13 and 17
for blood glucose determination. All the blood samples were collected in
fasted animals and 24 h after the preceding dose of drug or extract.

Glucose tolerance curve in alloxan-induced diabetic rats

Rats were made diabetic using alloxan as described. Rats were randomly
divided into three groups of 10 each on the 5th day following alloxan
injection. All the rats were administered glucose, 1 g/kg orally, after deter-
mining their FBG. Two groups of rats received either EE or chlorpropamide
orally along with the glucose. The third group served as control and received
vehicle along with glucose. Blood glucose levels were determined 1, 2 and 4 h
after glucose administration.

Glycogenesis in hemidiaphragm and glycogenolysis in liver of albino rat

Rats were fasted for 24 h before being killed by a blow to the back of
the head. The abdomen was then opened and the diaphragm carefully
excised and placed immediatelybin ice-cooled perfusion solution (BSS)
with the following composition: NaCl (0.687%), KC1 (0.04%), MgS04,
(0.014%), CaCl, (O.OZS%), NaH,P04 (0.014%) and NaHCO, (0.21%). Glu-
cose was added to another batch of this perfusate to make its concentration
up to 300 mg/ml. This fortified solution will hereafter be referred to as
GBSS. Hemidiaphragms were put into 2.0 ml of GBSS solution aerated for
5 min and then placed in Warburg cups. The cups were incubated in a water
bath at 37°C and shaken at a rate of 50 oscillations/min. At the end of
this experiment, glucose was assayed. The diaphragms were removed, rinsed
in water, dried in an oven at 100°C for 2 h and weighed. The final glucose
uptake during the incubation period was calculated in mg/g dry weight of
diaphragm. Similarly, liver slices were incubated in 2.0 ml of GBSS at
37°C. The final glucose concentration after the incubation period was
determined in mg/g of dry weight of liver.

Statistical analysis

Statistical significance of the difference of the means was calculated

using the Student’s t-test. LDsO and EDso estimations were calculated by
the method of Litchfield and Wilcoxon (1949).

Results

Acute toxicity and gross behavioral studies

In both mice and rats, EE at 25---50 mg/kg i.p. and 250--1000 mg/kg.
p.o. elicited slight sedation with no evidence of overt neurotoxicity. Higher
 179

doses (lOO.-200 mgfkg i.p.) and (2000-4000 mg/kg p.o.) produced hypo-
tonia followed by respiratory distress and some animals died due to respira-
tory failure. LDSO (95% confidence range) by the oral route in mice was
2580 (1912-3547) mg/kg and in rats (8670 (5570 -11770) mg/kg. LD,,
by the i.p. route in mice was 127 (91--.163) mg/kg and in rats 187 (133.7-
240.3) mgfkg.

Effect on blood pressure and respiration

In anesthetised rats, intravenous injection of EE (2.5-5 mg/kg. i.v.)
elicited a very transient (3.5 min) and insignificant fall in blood pressure
(5-8%). No alteration was observed either in the pressor responses of
epinephrine and norepinephrine or in the depressor resonses of acetyl-
choline and histamine. However, EE at 5 mg/kg i.v. produced a mild de-
crease in respiratory rate for a period of 30 min.

Isoia ted tissue preparations

EE at various concentrations (lo--500 pg/ml of bath) did not elicit a
contraction per se or inhibit contractions elicited by agonists like histamine
or acetylcholine in guinea pig ileum. Similarly, EE did not show any intrinsic
effects (even at highest concentration of 500 pg/ml of bath) and did not
block agonist responses on rat uterus and frog rectus abdominis muscle
preparations. EE at 100.-2500 pg did not show any effects on heart rate,
force of contraction or change in coronary flow in an isolated rabbit heart
prep~ation.

An ticonvulsan t, analgesic and anti-inflammatory studies

No analgesic or anticonvulsant activity of EE could be detected even at
1000 mg/kg p.o. by the methods employed in the present study. EE showed
inhibition of carrageenan edema in a dose-dependent manner. The oral
ED5,, (95% confidence range) for EE was 500 (382-655) mgfkg and for
phenylbutazone, a standard non-steroidal anti-inflammatory drug, 100
(83-120) mg/kg.

TABLE 2

EFFECT OF ETHANOL EXTRACT OF B. SA RTOR UM IN NORMAL RATS

Oral treatment Mean blood glucose concentration (mg% * S.E.M.)

(mgkg)
at 0 time ,--1 h +1 h +2h +4h +8h

Saline (-) 126 * 11 121 * 12 120 f 13 119 t 9 110 f 9

Extract (250) 126*11 110 f 7 108 i 12 105 f 11 100 f 10
Extract (500) 126 f 11 111 f 18 107 * 12 104 f 10 95 f: lo*
Extract (1000) 126 f 11 109 f 22 94 i 16 95 * 9* 92 f lo*

*Significant from saline control P < 0.05; each group consisted of 8-10 rats.
180

TABLE 3

EFFECT OF ETHANOL EXTRACT OF B. SARTORUM IN NORMAL RABBITS

Oral treatment Mean blood glucose concentration (mg% f S.E.M.)

(mgkg) -.
at 0 time --1 h 12h -14h r8h ~24 h
_..~ _
Saline (-) 126 t 18 124 t 18 125 * 10 121 t 8 118 1 10
Extract (250) 122 f 9 120t 9 109t 6 98 t 9* 121 t 13
Extract (500) 128 * 16 122 t 13 116: 8 92 f 10* 120t 8

*Significant from saline control I’ < 0.05; each group contained 8 rabbits.

Hypoglycemic/antidiabetic activity: normal rats

EE significantly reduced blood glucose levels in rats and rabbits with
maximum effects noted 8 h after administration (Tables 2 and 3).

Effect on epinephrine-induced hyperglycemia

Epinephrine treatment induced hyperglycemia in rats, and rats pretreated
with EE showed no significant reduction of this response. Similarly, the
standard antidiabetic drug, chlorpropamide, also failed to produce signifi-
cant inhibition of epinephrine-induced hyperglycemia in rats (Table 4).

Effect on alloxan-induced diabetes in rats

Alloxan treatment resulted in a marked increase in blood glucose levels
(a diabetic-like state). In such animals, EE (500 mg/kg p.o. daily for 12 days)
lowered blood glucose levels significantly from the 8th day of EE treatment.
Similarly, treatment with chlorpropamide reduced blood glucose level signif-
icantly from 8th day of chlorpropamide treatment (Table 5).

Effect on glucose tolerance in diabetic rats

Blood glucose levels of diabetic rats were significantly increased following
the oral administration of glucose (1 g/kg) on the 5th day. Pretreatment
with either EE or chlorpropamide significantly inhibited this elevated blood
glucose response indicating a changed pattern of glucose tolerance (Table 6).

TABLE 4

EFFECT OF ETHANOL EXTRACT OF B. SA RTORUM ON EPINEPHRINE-INDUCED

HYPERGLYCEMIA IN RATS

Oral treatment Mean blood glucose (mg% * S.E.M. )

(mgkg)
at 0 time -3 h A 30 min t 60 min

Saline ( -) 112 t 7 136t 8 140 f 9

Extract (1000) 118 t 8 121 t 10 128 f 8
Chlorpropamide (100) 118 t 6 125* 9 122 f 6

No significance noted from saline control; each group consisted of 10 rats.

 181

TABLE 5

EFFECT OF ETHANOL EXTRACT OF B. SARTORUM ON ALLOXAN-INDUCED

DIABETIC RATS

Blood glucose was determined on the 5th day after alloxan administration and drug/
extract treatment started that same day. Blood was collected on the 9th, 13th and
17th day following alloxan treatment (4, 8 and 12 days after the start of drug/extract
treatment).

Oral daily treatment Mean blood glucose concentration (mg% f S.E.M.)

(mg/kg) starting
at + 5 days + 5 days +9 days +13 days + 17 days

Saline (-) 246 * 15 234 f 14 221 f 18 220 f 19

Extract (500) 246 i 15 213 c 20 205 f ll* 195 f 12**
Chlorpropamide (50) 246 r 15 209 * 20 200 zt 12* 190 * 16**

*Significant at P < 0.05; **P < 0.01; 10 rats per experimental group.

Effect ofglycogenesis in hem~dia~hragms of albino rats

Addition of EE (20 mg/ml) or chlorpromamide (8 mg/ml) to the incu-
bation bath of hemidiaphragm showed a very highly significant enhancement
of the glucose uptake process by the diaphragms (Table 7). The effect of
EE and chlorpropamide was also investigated in diaphragms obtained from
alloxanised rats but no signific~t effects were recorded (Table 8).

Effect on glycogenolysis in liver slices of albino rats

EE showed a very highly significant inhibitory effect on the glycogeno-
lysis in liver slices (Table 9).

TABLE 6

EFFECT OF ETHANOL EXTRACT OF B. SARTORUM ON GLUCOSE TOLERANCE

IN ALLOXAN-INDUCED DIABETIC RATS

Oral treatment Mean blood glucose concentration (mg% r S.E.M.)

tmg/kgf
at 0 time -1 h +l h +2h +4h

Saline (-) 278 f 14 270 -f:12 260 f 10 248 +z13

Saline (--) + glucose 270 f 20 295 * 12 325 f 18 320 * 15
Extract (500) + 290 f 10 280 * 19 250 i 16* 240 +_24
glucose
Extract (1000) + 280 ?: 18 284 f 18 230 * 18** 220 t 21**
glucose
Chlorpropamide (100) 285 f 19 280 i 16 230 f 16** 228 i 16**
+ glucose

Significance from saline + glucose treatment: *P < 0.05; **P < 0.01 but no significance
noted from sahne control; 10 rata per experimental group.
182

TABLE 7

EFFECT OF ETHANOL EXTRACT OF B. SARTORUM ON GLUCOSE UPTAKE

OF ISOLATED HEMIDIAPHRAGM OF ALBINO RATS

The incubation period was 60 min at 37°C; N = 8 per treatment group.

Treatment Incubation Mean glucose uptake

concentration (mglg f S.E.M.)
(mg/ml)

Control 5.3 c 0.4

Extract 20 28.3 + 2.2*
Chlorpropamide 8 15.4 f 1.7*

*S&nificant at P < 0.001.

TABLE 8

EFFECT OF ETHANOL EXTRACT OF B. SARTORUM ON GLUCOSE UPTAKE

OF ISOLATED HEMIDIAPHRAGM OF ALLOXANISED ALBINO RATS

The incubation period was 60 min at 37°C. Hemidiaphragm of alloxanised rats were taken
7 days after alloxan treatment. No significance was recorded. N = 6 per treatment group.

Treatment Incubation Mean glucose

concentration uptake
(mg/ml) (mg/g f S.E.M.)

Control (with alloxan) 2.5 f 0.1

Control (without alloxan) _ 3.8 r 0.2
Extract (with alloxan) 20 5.0 f 0.2
Chlorpropamide (with alloxan) 8 4.0 2 0.1

TABLE 9

EFFECT OF ETHANOL EXTRACT OF B. SARTORUM ON ISOLATED LIVER

SLICES OF ALBINO RATS

The incubation period was 60 min at 37°C.

Treatment Incubation Mean glucose transfer

concentration (mg/g * S.E.M.)
(mg/ml)

Control - 40.0 f. 3.4

Extract 20 4.6 k 0.3*
Chlorpropamide 8 2.8 i 0.4*

*Significant at P < 0.001; N = 8 per treatment group.

 183

Discussion

Acute toxicity studies with an ethanolic extract of B. sartorum suggest

that the extract is more toxic intraperitoneally than orally in both mice
and rats. Orally the extract showed dose-dependent hypoglycemic activity
in normal rats and rabbits with maximum activity observed around 8 h
after treatment and with a return to normal over a period of 24 h (Tables
2 and 3). Glucose tolerance in rats was significantly altered with an effect
comparable to that of chlorpropamide. The effect of chlorpropamide on
glucose tolerance has been attributed to enhanced activity of p-cells of
pancreas resulting in secretion of larger amounts of insulin (Best and Taylor,
1959). Alternatively, inhibition of adrenocortical activity by chlorpropamide
may facilitate the effect of insulin on hexokinase-mediated glucose utiliz-
ation by tissues because adrenal cortical steroids are known to antagonise
this effect on hexokinase (Colwick et al., 1947). Therefore, it is possible
that the EE may also affect glucose metabolism through similar mechan-
isms.
Alloxan is known to destroy p islets of Langerhans resulting in a diabetic
state. In the present study, a submaximal dose of alloxan was employed
in order to produce partial destruction of S-cells of pancreas simulating
the mild diabetes of adulthood. Administration of EE elicited a significant
hypoglycemic effect in alloxan-diabetic rats and this effect was similar to
that seen with chlorpropamide. These results suggest that the hypoglycemic
effect of the ethanol extract may be through increased release of insulin
from the remaining islets of Langerhans. The hypoglycemic action of the
ethanol extract was abolished on administering higher doses of alloxan
which destroyed completely the pancreatic P-cells (data not shown). Thus,
it seems possible that the mode of action of the ethanol extract of B. sar-
torum is through an enhanced secretion of insulin. However, it has also
been reported (Gandhi and Jindal, 1971, quoting work of Caren and Corbo,
1957) that on administration of sulphonylurea compounds to depancreatised
dogs shortly before and after a single intravenous injection of soluble insulin
results in a greater fall in blood glucose levels lasting for a longer period as
compared to the effects of insulin alone. Accordingly, we have conducted
some in vitro experiments on rat diaphragms for glucose uptake and on liver
slices for glycogenolysis. Results indicate that the extract at 20 mg/ml and
chlorpropamide at 8 mg/ml had significant effects on the glucose uptake
process in normal muscles. However, neither extract nor chlorpropamide
had a significant effect on alloxanised diaphragm as compared to normal
diaphragms. Experiments with liver slices indicate that the extract and
chlorpropamide showed an inhibitory effect against conversion of liver
glycogen into blood glucose as compared to control group.
These findings suggest that the extract also has some peripheral action
such as enhancing glucose uptake in the muscles and inhibiting conversion
of liver glycogen into blood glucose in a manner similar to that of tolbu-
tamide (Anderson et al., 1956; 1957; Clark et al., 1956; Vaughan, 1959).
184

The extract also showed dose-related anti-inflammatory activity in rats.

It has been reported that the oleanane group of triterpenoids possess anti-
inflammatory activity (Gupta et al., 1969). Furthermore, Bhargava et al.
(1970) have reported anti-inflammatory activity in animals for saponin
of trihydroxy bassic acid isolated from other plants. We have isolated and
identified bassic acid from the ethanol extract and it is likely that bassic
acid may be responsible for the anti-inflammatory activity observed in the
present study. However, it is yet to be investigated whether or not the
bassic acid component of the ethanol extract of B. sartorum is responsible
for the hypoglycemic effect observed in the present study.
The ethanol extract did not elicit any significant effects on the cardio-
vascular system. The extract also failed to show any intrinsic effects or
antagonism of standard agonist responses when tested on isolated smooth,
skeletal and cardiac muscles.
In conclusion, it may be stated that the ethanol extract of B. sartorum
shows promising hypoglycemic and anti-inflammatory activity in animal
experiments. The ethanolic extract contains bassic acid, a triterpene acid,
which has been isolated and identified from this plant for the first time.
Further experiments are required to show whether or not bassic acid is
responsible for the observed hypoglycemic effects.

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