Fitoterapia 100 (2015) 110–117

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Fitoterapia
journal homepage: www.elsevier.com/locate/fitote

Protective effects of pogostone from Pogostemonis Herba

against ethanol-induced gastric ulcer in rats
Haiming Chen a,1, Huijun Liao c,1, Yuhong Liu a, Yifeng Zheng a, Xiaoli Wu a,d, Zuqing Su a, Xie Zhang a,
Zhengquan Lai c, Xiaoping Lai a,b, Zhi-Xiu Lin c,⁎, Ziren Su a,b,⁎⁎
a
College of Chinese Medicines, Guangzhou University of Chinese Medicine, Guangzhou 510006, People's Republic of China
b
Dongguan Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Dongguan 523808, People's Republic of China
c
School of Chinese Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China
d
Faculty of Health Sciences, University of Macau, Macau 999078, People's Republic of China

a r t i c l e i n f o a b s t r a c t

Article history: We examined the protective effect of pogostone (PO), a chemical constituent isolated from
Received 5 September 2014 Pogostemonis Herba, on the ethanol-induced gastric ulcer in rats. Administration of PO at doses of
Accepted in revised form 18 November 2014 10, 20 and 40 mg/kg body weight prior to ethanol ingestion effectively protected the stomach
Accepted 21 November 2014 from ulceration. The gastric lesions were significantly ameliorated by all doses of PO as compared
Available online 3 December 2014
to the vehicle group. Pre-treatment with PO prevented the oxidative damage and the decrease of
prostaglandin E2 (PGE2) content. In addition, PO pretreatment markedly increased the mucosa
Keywords: levels of glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT), and decreased
Pogostone gastric malonaldehyde (MDA), relative to the vehicle group. In the mechanistic study, significant
Ethanol
elevation of non-protein-sulfhydryl (NP-SH) was observed in the gastric mucosa pretreated by
Gastric ulcer
PO. Analysis of serum cytokines indicated that PO pretreatment obviously elevated the decrease of
Antioxidant
Anti-inflammatory interleukin-10 (IL-10) level, while markedly mitigated the increment of interleukin-6 (IL-6) and
Rats tumor necrosis factor alpha (TNF-α) secretions in ethanol-induced rats. Taken together, these
results strongly indicate that PO could exert a gastro-protective effect against gastric ulceration,
and the underlying mechanism might be associated with the stimulation of PGE2, improvement of
antioxidant and anti-inflammatory status, as well as preservation of NP-SH.
© 2014 Elsevier B.V. All rights reserved.

1. Introduction neutrophils, reduction in blood flow, induction of oxidative

Peptic ulcers are pathological lesions in the gastrointestinal
tract that usually occur in the stomach and duodenum [1].
The gastric ulcer is characterized by necrosis, infiltration of
Abbreviations: CAT, catalase; GSH, glutathione; H&E, hematoxylin and
eosin; IL-6, interleukin-6; IL-10, interleukin-10; MDA, malonaldehyde; NP-SH,
non-protein-sulfhydryl; NSAIDs, non-steroidal anti-inflammatory drugs; TNF-α,
tumor necrosis factor alpha; PO, pogostone; PGE2, prostaglandin E2; SOD,
superoxide dismutase.
⁎ Corresponding author. Tel.: +852 3943 6347; fax: +852 2603 7203.
⁎⁎ Correspondence to: Z. Su. Tel.: +86 20 39358517; fax: +86 20 3935 8390.
E-mail addresses: linzx@cuhk.edu.hk (Z.-X. Lin), suziren@gzucm.edu.cn
(Z. Su).
1
These two authors contributed equally to this work.
stress, and secretion of inflammatory mediators [2,3].
Gastric ulcer is one of the major gastrointestinal disorders
with increasing incidence and prevalence globally [4,5]. It is
estimated that 14.5 million people worldwide are affected by
gastric ulcers in 2007, with a mortality of 4.08 million [6–8]. It is
well-known that gastric lesions occur primarily due to the
imbalance between the harmful and gastro-protective factors
of the gastric mucosa [9,10]. Excessive drinking habits, poor
diets, stress, smoking, Helicobacter pylori and excessive inges-
tion of non-steroidal anti-inflammatory drugs (NSAIDs) all
contribute to peptic ulcer disease [8,11,12].
To date, a great number of synthetic drugs have been used for
the treatment of gastric ulcers, such as anti-acids, proton pump
inhibitors, anticholinergics and histamine receptor antagonists

http://dx.doi.org/10.1016/j.fitote.2014.11.017
0367-326X/© 2014 Elsevier B.V. All rights reserved.
 H. Chen et al. / Fitoterapia 100 (2015) 110–117
[13]. However, many of these drugs not only can produce
undesirable adverse effects, but also involve high cost in gastric
ulcer patients [14,15]. Natural products of plant origin that
may present fewer side effects are emerging as a promising
therapeutic resource for the development of new drugs in the
management of gastrointestinal diseases. To this extent, we look
into natural medicinal plants for drug discovery.
Pogostemonis Herba, known as “Guang-Huo-Xiang” in
Chinese, is originated from the dried aerial part of Pogostemon
cablin (Blanco) Benth. (Labiatae). Its therapeutic functions in
Chinese medicine are to remove dampness, relieve summer-
heat and exterior syndrome, stop vomiting and stimulate
appetite [16]. Clinically, Pogostemonis Herba has been widely
used by traditional Chinese physicians to treat a wide array of
medical conditions such as common cold, nausea, diarrhea,
headache and fever since time immortal [17]. Moreover, it is
also an important component herb of many popular herbal
formulae, such as Baoji Pill and Huoxiang Zhengqi Liquid, for
the treatment of gastrointestinal diseases.
Pogostone (PO, C12H16O4, the chemical structure is shown
in Fig. 1) is the major chemical constituent of Pogostemonis
Herba and is largely responsible for the intensive aromatic odor
of the essential oil of this herb [18,19]. This compound has been
demonstrated to exert potent antibacterial [20], anti-fungal
[21] and anti-Candida [22] activities. Patchouli alcohol, another
major ingredient of Pogostemonis Herba, was reported to exert
gastro-protective effect in our previous work [23]. However, so
far the antiulcerogenic activity of PO has not been reported in
the literature. Therefore, our present study aimed to evaluate
the antiulcerogenic potential of PO using the ethanol-induced
gastric ulcers in rats as an experimental model, as well as to
determine the effects of PO on gastric biochemical parameters
and to elucidate its mechanisms of action.
2. Materials and methods
2.1. Plant materials and reagents
The aerial parts of P. cablin were collected in September
2012 in Maoming, Guangdong province, China. It was authen-
ticated by one of the authors (Xiaoping Lai, an experienced
Pharmacognosist) at the School of Chinese Materia Medica,
Guangzhou University of Chinese Medicine, where a voucher
specimen (No. 120911) was deposited.
Lansoprazole tablets were purchased from Tuobin Pharma-
ceutical Factory (Shantou, China) and ethanol was from
Guangzhou Chemical Reagent Factory (Guangzhou, China).
The ultrapure water was purified using a Milli-Q gradient water
purification system (Millipore, Bedford, MA, USA). All other
chemicals and reagents were analytical grade.
Fig. 1. The chemical structure of pogostone (PO).
111
2.2. Extraction and isolation of PO
PO was isolated from P. cablin as previously described [22].
The extraction and isolation procedure was as follows. Briefly,
the dried aerial parts of P. cablin (6 kg) were exhaustively
extracted through water–steam distillation. Essential oil
(20.4 g) was obtained from P. cablin and dissolved in ethyl
acetate (100 ml), and then was extracted five times with 4%
NaOH (100 ml). The five alkaline extracts were pooled and 10%
HCl was added to produce a pH 2 solution. The solution was
extracted three times with ethyl acetate (400 ml); then the
ethyl acetate extracts were combined, washed five times with
distilled water (800 ml), and the organic layer was evaporated
in vacuo to get yellow oily liquid. After crystallization from
normal hexane, white PO crystal (246.8 mg, yield 0.0041%) was
finally obtained. PO was lipid soluble with melt point ranging
from 32.6 to 33 °C and molecular weight of 224. Its chemical
structure was identified by comparing its spectral data (MS, 1H-
and 13C-NMR) with those published previously [21,24], and its
purity was above 98% as determined by HPLC-UV using a
previously described method [25].
2.3. Animals
Male Sprague–Dawley rats (6–7 weeks old, 180–220 g)
were obtained from Laboratory Animal Center of Guangzhou
University of Chinese Medicine (Guangzhou, China). Rats were
housed in an environmentally controlled condition (22 ± 2 °C,
relative humidity of 50 ± 5%) with a 12-h light/dark cycle and
allowed free access to food and water. All rats were housed in
cages with raised floors of a wide mesh to prevent coprophagy
and fasted for 24 h prior to experimentation. Experimental
protocols used in the present study were approved by the
Animal Experimental Ethics Committee of Guangzhou Univer-
sity of Chinese Medicine (Guangzhou, China). All efforts were
made to minimize animal suffering and to reduce the number
of animals used in the experiments.
2.4. Administration and dose selection
Male Sprague–Dawley rats were randomly divided into six
groups, with each containing six animals. The normal and ulcer
control groups received distilled water and vehicle respectively
throughout the course of the experiment. The prevention
groups received lansoprazole (30 mg/kg) and different doses of
PO (10, 20 and 40 mg/kg) dissolved in physiological saline, as
described in the literature [26], for a period of 7 days. PO
dosage was selected based on a preliminary dosing experiment
on ethanol induced ulceration.
2.5. Ethanol-induced gastric ulcers
All rats were fasted for 24 h with free access to drinking
water and were treated as described in Section 2.3 for the last
time before the initiation of the ethanol-induced ulceration.
One hour after this treatment, the rats except those in the
normal group received an oral administration of 1 mL of
absolute ethanol. One hour after ethanol administration, all rats
were euthanized and the blood samples were obtained with no
addition of anticoagulants and centrifuged at 740 g for 10 min
to obtain serum for biochemical analysis. Meanwhile, their
112 H. Chen et al. / Fitoterapia 100 (2015) 110–117
stomachs were removed rapidly and opened along the greater
curvature and rinsed with cold saline to remove the gastric
contents and blood clots. The flattened stomach samples
were photographed and the ulcer area (mm2) was measured
using ImageJ software (developed by the National Institutes
of Health, USA). The inhibition percentage was calculated
using the following formula: [(Ulcer Area(Vehicle) − Ulcer
Area(Treated)) / Ulcer Area(Vehicle)] × 100%.
The stomach samples were scrapped after the scans and
rapidly frozen with liquid nitrogen. Finally, all stomach samples
were stored at −80 °C until biochemical analyses.
2.6. Histological analysis
Stomach samples removed from each rat were fixed in
10% buffered formalin and embedded in paraffin. Paraffin
sections were then cut to a thickness of 5 μm and stained
with hematoxylin and eosin (H&E) for histological evalua-
tion according to standard procedures [27].
2.7. Cytokines evaluations
The levels of cytokines (IL-6, IL-10 and TNF-α) in the serum
were evaluated using commercial enzyme-linked immunosor-
bent assay (ELISA) kits (eBioscience, USA) as per the
manufacturer's instructions [28]. The absorbance was read at
450 nm with a microplate spectrophotometer (Multiskan GO,
Thermo Fisher Scientific, USA).
2.8. Measurement of glutathione (GSH), superoxide dismutase
(SOD), malonaldehyde (MDA) level, and catalase (CAT) activity
Stomach tissues stored at −80 °C were homogenized in
homogenization Tris-buffer (20 mM, pH 7.5) on ice using Ultra
Turraks Homogenizer (IKA, Germany) and then were centri-
fuged at 11,940 g at 4 °C for 10 min. The supernatants were
used to determine the activities of CAT and SOD, and levels of
GSH and MDA. The concentration of protein in the supernatants
was determined by the Bradford method using bovine serum
albumin (BSA) as a standard. The activities of CAT and SOD
and the levels of GSH and MDA were determined using
commercial assay kits according to the manufacturer's instruc-
tions (Jiancheng Company, Nanjing, China) [29,30].
2.9. Determination of non-protein sulfhydryls (NP-SH)
Tissue homogenates were prepared from rats of the
ethanol-induced gastric ulcer as mentioned in Section 2.8.
Non-protein sulfhydryl (NP-SH) content was determined as
previously described [31].
2.10. Determination of prostaglandin E2 (PGE2)
PGE2 levels were determined in stomach tissues obtained
from the ethanol-induced gastric ulcer. The stomach tissue was
homogenized and centrifuged as described before and the
supernatant was used for determination of PGE2 by using an
enzyme immunosorbent kit (R&D Systems, Abingdon, UK) [23].
The optical densities were measured at 450 nm and the results
were expressed as ng/g protein.
2.11. Statistical analysis
The results were expressed as mean ± SEM and all statistical
analyses were performed with Statistical Product and Service
Solutions (SPSS) software. The statistical significance of differ-
ences for each parameter among groups was analyzed using a
one-way analysis of variance (ANOVA) followed by Dunnett's
test. A value of P b 0.05 was considered statistical significant.
3. Results
3.1. Ethanol induced gastric ulcers
The ulcer control group presented severe mucosal injury
with an average ulcer area of 260.47 ± 16.89 mm2. A
significant decrease (P b 0.01) in ulcer area was observed in
the lansoprazole-treated group with an average area of 3.38 ±
1.13 mm2 (98.70% inhibition). For the PO-treated groups, the
ulcer area was significantly attenuated (P b 0.01) in a dose-
dependent manner. The 40 mg/kg of PO group exhibited the
smallest ulcer area (12.90 ± 0.87 mm2) and the highest
inhibition (95.05% inhibition). The ulcer areas of the 20
and 10 mg/kg PO groups were 60.32 ± 3.83 and 143.60 ±
7.46 mm2 (76.84% and 44.87% inhibition) respectively. A
representative stomach of each group is shown in Fig. 2, and
the ulcer areas are listed in Fig. 3.
3.2. Histological evaluations
Results of histological analyses of the gastric mucosa are
depicted in Fig. 4. Rats pre-treated with the vehicle (physio-
logical saline) showed severe damage to the gastric epithelium.
In the histological observation of gastric ulcer induced by
ethanol, rats pre-treated with PO (10 and 20 mg/kg) showed
less mucosal damage when compared with the vehicle group.
Rats pre-treated with PO at 40 mg/kg showed normal histology
or only very superficial lesions, and the observation was
comparable to those treated with lansoprazole.
3.3. Effect of PO on serum cytokines
The serum levels of TNF-α and IL-6 were accentuated while
IL-10 was reduced in the rats ulcerated by ethanol relative to
the control group. However, PO at dose of 20 and 40 mg/kg
significantly reduced the levels of the pro-inflammatory
cytokines TNF-α (P b 0.05) and IL-6 (P b 0.01). Although the
low dose did not achieve statistical significance, decreases in
TNF-α and IL-6 productions were also observed compared with
the vehicle group. And pretreatment with PO at all tested doses
(P b 0.05, P b 0.05 and P b 0.01, respectively) augmented the
anti-inflammatory factor IL-10 level in a dose-dependent
manner relative to the vehicle group (Table 1).
3.4. Effect of PO on SOD, GSH, CAT and MDA levels in the stomach
tissue of the ethanol-treated rats
Table 2 shows the results of SOD, GSH, CAT and MDA assays.
After oral administration with PO of three doses, SOD and GSH
activities were elevated obviously (P b 0.05, P b 0.01 and
P b 0.01, respectively), which was in concerted with the dose-
dependent decrease in MDA levels in the stomach tissue
 H. Chen et al. / Fitoterapia 100 (2015) 110–117
Fig. 2. Effects of PO on the macroscopic appearance of the gastric mucosa in the ethanol-induced gastric lesions in rats. (A) Control group; (B) Vehicle group;
(C) Lansoprazole group (30 mg/kg); (D) PO (10 mg/kg) group; (E) PO (20 mg/kg) group; and (F) PO (40 mg/kg) group.
(P b 0.05, P b 0.01 and P b 0.01, respectively). While PO at doses
of 20 and 40 mg/kg significantly increased the CAT activity
(P b 0.05, P b 0.05) in parallel to the vehicle group. The low
dose also led to an increment in CAT activity, though the
variation did not reach the statistical significance. Herewith, the
observation indicated that PO might attenuate the ethanol-
induced changes via regulation of oxidant–antioxidant balance.
Among all the tested doses of PO, 40 mg/kg exhibited the best
antioxidant effect.
Fig. 3. Effects of lansoprazole (30 mg/kg) and PO (10, 20 and 40 mg/kg) on the
gastric ulcer area (mm2) in rats subjected to ethanol treatment. The results
were expressed as mean ± SEM and analyzed by ANOVA followed by Dunnett's
test, **P b 0.01 vs. control group.
113
3.5. Effect of PO on non-protein-sulfhydryl (NP-SH) and prosta-
glandin E2 (PGE2) levels
Administration of rats with PO significantly (P b 0.05)
restored the depletion of NP-SH caused by ethanol pretreat-
ment (Table 3). The decreased level (P b 0.01) of PGE2 in the
vehicle group when compared to that of the control group
provided evidence that ethanol treatment reduced the PGE2
production. Table 3 shows that PO was able to maintain a high
PGE2 level in the rats despite being treated with ethanol.
4. Discussion
The present study aimed to evaluate the anti-ulcer activity
of PO using an ethanol-induced experimental gastric ulcer
model and to investigate its underlying mechanisms of the
action associated with its anti-ulcer activity.
Alcohol consumption can produce acute hemorrhagic
gastric erosions, and excessive ingestion can result in gastritis
characterized by mucosal edema, sub-epithelial hemorrhages,
cellular exfoliation, and inflammatory cell infiltration [32,33],
all are the hallmarks of an acute inflammatory reaction.
However, oral administration of PO effectively reversed the
ethanol-induced gastric injury in a dose-dependent manner,
with significant reduction of the gastric ulcer area. The
protective activity of PO was also ascertained with lesser
gastric damage magnitude of the rats in PO-treated groups than
that of the counterparts in the vehicle group (Fig. 2B). The
protective effect of PO towards the rat stomach mucosa
exhibited in a dose-dependent manner became apparent
(Fig. 2D–F). A week of pretreatment with PO had notably
inhibited the mucosal damage of gastric wall (Fig. 4D–F) while
114 H. Chen et al. / Fitoterapia 100 (2015) 110–117

Fig. 4. Histological evaluation of the ethanol-induced gastric mucosa damage in rats (H&E staining; magnification 100×). (A). Control stomach: intact gastric epithelium
with organized glandular structure and normal submucosa could be seen; (B)–(F) ethanol-induced ulcer. (B) Rats pre-treated with vehicle: *indicates damaged
mucosal epithelium with disrupted glandular structure and arrow depicts edema of submucosa and inflammatory infiltrate; (C) lanoprazole 30 mg/kg; (D) PO
10 mg/kg; (E) PO 20 mg/kg; (F) PO 40 mg/kg. (C), (D), (E) and (F) depict a recovery in mucosal epithelium and reorganized glandular structure as well as improvement
of edema by lansoprazole and PO treatment respectively.

the ulcerated control rats (Fig. 4B) showed severe disruption to
the surface epithelium, necrotic lesions penetrated deeply into
mucosa, and extensive edema of submucosal layer. This study
amply demonstrated that PO had gastroprotective action
against the ethanol-induced gastric ulcer.
Interleukins play a vital role in the regulation of the mucosal
defense barrier. Ethanol ingestion may activate the innate
immune system leading to changes in the level of inflammatory
cytokines, such as TNF-α, IL-10 and IL-6 [5]. Previous findings
implicated that the levels of pro-inflammatory cytokines IL-6
and TNF-α remarkably increased in the gastric tissue of the
ethanol-induced ulcer [34,35] while anti-inflammatory factor
IL-10 was significantly reduced in gastric ulceration [36].
TNF-α, a representative inflammatory cytokine with
pleiotropic functions, is closely involved in the process of
inflammation. The evidence that an aberrant high level of
TNF-α is detected in the serum of rats with inflammatory
diseases including severe mucosal inflammation [37] and

Table 1
Effect of PO on the serum levels of TNF-α, IL-6 and IL-10 in rats with the ethanol-induced gastric ulcers (n = 6).

Group Dose TNF-α IL-6 IL-10

(mg/kg) (pg/mg protein) (pg/mg protein) (pg/mg protein)

Control – 11.49 ± 0.85** 6.47 ± 0.45** 18.44 ± 0.96**

Vehicle – 15.53 ± 0.80 10.30 ± 0.50 12.97 ± 0.88
Lansoprazole 30 11.15 ± 0.68** 7.58 ± 0.73** 17.14 ± 0.80**
PO 10 13.12 ± 1.63 8.38 ± 0.61 14.22 ± 0.88*
PO 20 12.15 ± 0.66* 8.02 ± 0.45** 15.64 ± 0.93*
PO 40 11.66 ± 1.28* 7.92 ± 0.47** 16.87 ± 0.96**

The results were expressed as mean ± SEM and analyzed by ANOVA followed by Dunnett's test, **P b 0.01, *P b 0.05 vs. the vehicle group.
 H. Chen et al. / Fitoterapia 100 (2015) 110–117 115

Table 2
Effect of PO on SOD, GSH, CAT and MDA levels in the stomach tissue of the ethanol-treated rats.

Group Dose SOD GSH CAT MDA

(mg/kg) (pg/mg protein) (pg/mg protein) (pg/mg protein) (pg/mg protein)

Control – 8.12 ± 0.48** 10.95 ± 0.34** 6.25 ± 0.65** 1.35 ± 0.16**

Vehicle – 5.35 ± 0.71 6.20 ± 0.49 3.58 ± 0.32 2.50 ± 0.22
Lansoprazole 30 8.37 ± 0.42** 10.00 ± 0.65** 6.18 ± 0.68** 1.65 ± 0.19**
PO 10 7.23 ± 0.50* 8.25 ± 0.25* 4.63 ± 0.43 1.90 ± 0.08*
PO 20 7.83 ± 0.34** 8.72 ± 0.69** 5.40 ± 0.60* 1.71 ± 0.20**
PO 40 8.17 ± 0.45** 9.16 ± 0.75** 5.40 ± 0.65* 1.63 ± 0.12**

The results were expressed as mean ± SEM and analyzed by ANOVA followed by Dunnett's test, **P b 0.01, *P b 0.05 vs. the vehicle group.

in gastric lesion specimens obtained from patients [38], ethanol markedly increased MDA level, accompanied by a
strongly supports the hypothesis that TNF-α has detrimental decrease of GSH, CAT and SOD activities, all of which are
effects, such as inducing tissue injury and inflammation. IL-6, endogenous antioxidants. Our data support a critical role of
another key pro-inflammatory cytokine, is known to partici- oxidative stress in the pathogenesis of the ethanol-induced
pate in inflammation process and to modulate the expression gastric ulcer. Nevertheless, pretreatment with PO resulted in
of genes involved in cell cycle progression and inhibition significant increases in the activities of SOD and the levels of
of apoptosis [39]. IL-10 plays an important role in down- GSH, as well as a decrease in MDA formation, indicating its
regulating inflammatory cascade by enhancing the production antioxidant activity. Our experimental results indicate that PO
of anti-inflammatory cytokines, mitigating the production potentially exerted gastroprotective effect via an antioxidant
of pro-inflammatory cytokines and preventing autoimmune mechanism.
pathologies [40–42]. Therefore, the possible changes in the It has been reported that the endogenous NP-SH is
level of cytokines IL-6, TNF-α and IL-10 were investigated important in the maintenance of mucosal integrity against the
(Table 1). Results indicate that the observed increase in serum ethanol-induced gastric injury [47]. Its continuous adherence
IL-6 and TNF-α levels and decrease in IL-10 production can be to mucus layer is a barrier to luminal pepsin and creates a
attributable to the necrotizing effects of ethanol. However, the stable, undisturbed layer to support the surface neutralization
inflammatory status had been improved favorably in the of acid, preventing the underlying mucosa from proteolytic
animals pretreated with lansoprazole and PO at all doses. digestion [48]. If disulfide bridges, which can connect the
Despite the widely accepted notion that alcohol abuse leads mucus subunits, are reduced, the mucus may become water-
to detrimental consequences in the gastrointestinal tract, soluble and easily withdrawn by ulcerogenic agent, including
the mechanisms underlying it still remain obscure. There is ethanol [49]. Our study indicated that PO-treated groups
growing evidence that ethanol-induced gastric mucosal injury effectively elevated the gastric NP-SH content when compared
is closely related to the increased ROS level and the major to the vehicle group. PO significantly increased basal levels of
source of ROS is from the activated neutrophils [43]. NP-SH groups, confirming the involvement of these groups in
On the other hand, organisms per se have enzymatic and the gastroprotective effect.
non-enzymatic defenses, including GSH, SOD and CAT against PGE2, which is crucial in the regulation of gastric mucus
the ROS-induced lipid peroxidation [44]. GSH and SOD are secretion, can be reduced by ethanol [50]. PGE2 acts via
known to be able to scavenge superoxide, hydrogen peroxide, improving blood flow to maintain the cellular integrity in the
hydroxyl and lipid peroxyl radicals, with a consequence of mucosa [50,51], increasing mucus secretion, and bicarbonate
attenuating the tissue damage. CAT as preventive antioxidant and sulfhydryl compounds to strengthen the resistance of
triggers the rapid conversion of peroxyl radical into biologically gastric mucosal cells to the necrotizing effect of strong irritants
safe substances, like water [45]. MDA, an index of lipid [52,53]. Our results showed that PO was able to increase PGE2
peroxidation, can usually quantify to identify lipid peroxidation levels in a dose-dependent manner after the administration of
[46]. Thus, to address the role of oxidative stress in our model, ethanol, which might explain why PO exhibited a reducing
we assessed several oxidant–antioxidant parameters in the effect on ethanol-induced ulceration in a dose-dependent
gastric tissues of rats. The experimental results showed that fashion.
In conclusion, the results of the present study amply
demonstrated that PO pre-treatment was able to exert
Table 3 protective effects in the ethanol-induced gastric ulcer
Effect of PO on the ethanol-induced changes in NP-SH and PGE2 content in
gastric tissue homogenate.
model. PO administration not only significantly increased
CAT, SOD and GSH activities and decreased MDA level in
Group Dose NP-SH (ng/g protein) PGE2 (ng/g protein) gastric tissue, but also reduced the secretions of pro-
(mg/kg)
inflammatory mediators such as IL-6 and TNF-α and raised
Control – 53.60 ± 6.60* 73.02 ± 3.52* the level of anti-inflammatory cytokine IL-10 in serum in
Vehicle – 31.87 ± 4.27 59.38 ± 4.61
rats exposed to ethanol. The experimental findings render
Lansoprazole 30 51.13 ± 5.25* 73.00 ± 3.98*
PO 10 46.29 ± 6.08 71.21 ± 2.99* PO as a promising chemical constituent for the treatment of
PO 20 51.86 ± 6.36* 72.71 ± 3.58* gastric ulcer. Moreover, the elucidation of the underlying
PO 40 52.91 ± 6.90* 74.14 ± 3.17** mechanisms of action also helps put the traditional use of
The results were expressed as mean ± SEM and analyzed by ANOVA followed Pogostemonis Herba for gastrointestinal diseases on a solid
by Dunnett's test, **P b 0.01, *P b 0.05 vs. the vehicle group. scientific footing.
116 H. Chen et al. / Fitoterapia 100 (2015) 110–117
Conflict of interest
The authors declare that they have no competing interests.
Acknowledgments
This work was supported by grants from the National
Natural Science Foundation of China (No. 81173534), Guang-
dong International Cooperation Project (No. 2012B050300002),
Science and Technological Program for Dongguan's Higher
Education, Science and Research, and Health Care Institutions
(No. 2012105102009), Ph.D. Programs Foundation of Ministry
of Education of China (No. 20134425110009) and Science
and Technology Innovation Project of Guangdong Provincial
Department of Education (No. 2013KJCX0045), and Science and
Technology Planning Project of Guangdong Province (No.
2012A080202002), and Central Finance of China in Support of
the Development of Local Colleges and University [Educational
finance Grant No. 276(2014)], and Science and technology
cooperation projects among Hong Kong, Macao and Taiwan
(No. 2014DFH30010).
Appendix A. Supplementary data
Supplementary data to this article can be found online at
http://dx.doi.org/10.1016/j.fitote.2014.11.017.
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