- RESEARCH ARTICLE -
Antiulcer Potential of the Ethanolic Extract of
Aerva Persica Merrill Root in Rats
Neeru Vasudeva*, Payal Sethi, Surendra Kr. Sharma, Suresh Kumar,
Department of Pharmaceutical Sciences, Guru Jambheshwar University of Science and Technology, Hisar, India
Available online Feb 10, 2012
Received: May 10, 2011
Accepted: Sep 9, 2011
The ethanol extract of the roots of Aerva persica (Burm f) Merrill (Amaranthaceae) was
investigated to determine its antiulcer and in vivo antioxidant activities in albino Wistar
rats. Ulcers were induced by ethanol and pylorus ligation. The extract was administered
at the dose of 200 mg/kg orally, p.o. for 15 consecutive days. The ulcer index of the ethanol
extract was found to be significantly reduced compared with control animals. The effect
was also assessed by determining the free acidity, pepsin activity, total carbohydrate
(TC), and protein content (PK) in control, standard, and test group animals. The in vivo
antioxidant activity was evaluated by determining the reduced glutathione level (GSH)
and malondialdehyde (MDA) level in the tissue homogenates. The results reveal the signif-
icant reduction in the level of malondialdehyde and the increase in the level of reduced
glutathione in the rats that received the ethanolic extract. Furthermore, histopathological
studies have shown that pretreatment with the ethanolic extract of the roots of A persica
reduces (100%) ethanol- and pylorus ligation-induced hemorrhagic necrosis in rats.
Peptic ulcer disease (PUD), which includes gastric and
duodenal ulcers, is the most prevalent gastrointestinal
disorder and requires a well-targeted therapeutic strategy.
The pathophysiology of PUD involves an imbalance between
offensive (acid, pepsin, and Helcobacter pylori) and
defensive factors (mucin, prostaglandin, bicarbonate,
nitric oxide, and growth factors) [1,2]. The most common
sites for ulcers are the stomach and the first few centi-
meters of the duodenum. Acute peptic ulcers involve
tissues down to the depth of the submucosa, and the lesions
may be single or multiple. Reasons for the development of
emotional disturbance, and postsurgical complications.
Chronic peptic ulcers penetrate through the epithelial and
* Corresponding author. Department of Pharmaceutical Sciences, Guru Jambeshwar University of Science and Technology, Hisar, Haryana-
Copyright ª 2012, International Pharmacopuncture Institute
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J Acupunct Meridian Stud 2012;5(2):80e86
muscle layers of the stomach wall. Complications of peptic
ulcers include hemorrhage, perforation, pyloric stenosis,
and the development of malignant tumors . Poor diges-
tion and elimination, improper metabolism, mental and
physical stress, and difficult to digest food enhance the
development of ulcers. A number of drugs are available for
the treatment of peptic ulcers, but clinical evaluation of
these drugs indicates high incidences of relapse, side
effects, and drug interactions. These negative effects are
the rationale for the development of new antiulcer drugs
and the search for novel molecules in plants, such as Oci-
mum sanctum, Azadirachta indica, Asparagus racemosus,
Musa sapientum, Centella asiatica, Bacopa monnieri, and
Bidens pilosa, that offer could better protection and
decreased relapse . In view of the above, the present
study was performed to investigate the antiulcer activity of
the ethanolic extract of the roots of Aerva persica. The
effects of this plant were also confirmed by studying its
in vivo antioxidant effects; antioxidants, such as malon-
dialdehyde and glutathione, seem to have protective roles
against gastric ulcers and carcinomas .
2. Materials and methods
Albino Wistar rats of either sex, weighing between 150e
250 g, were used to determine the antiulcer activity of
the ethanolic extract. All animals were acclimatized and
maintained under standard laboratory conditions before the
start of the experiments. They were fed a normal diet and
provided water ad libitum. The institutional animal ethics
committee of Guru Jambheshwar University of Science and
Technology, Hisar, India (Reg. No. 0436) approved the
2.2. Plant materials and preparation of the extract
A persica was collected during the month of July from Hisar,
Haryana, India. The plant was taxonomically identified and
authenticated by Dr. H.B. Singh, head of the Raw Materials
and Herbarium Museum, National Institute of Science
New Delhi, India. The specimens were deposited in the
herbarium section of the Pharmacognosy Division, Depart-
ment of Pharmaceutical Sciences, Guru Jambheshwar
University of Science and Technology, Hisar, India for
further reference. The powdered roots were extracted with
ethanol (95%) using the continuous hot extraction method
for 72 hours [5,6]. The extracts were filtered, concen-
trated, and dried using a rotary evaporator. The percentage
yield of the ethanolic extract of the root was found to be
2.25%. The dried extract was stored at 4?C until further
use. The extract was suspended in 2% weight/volume
Tween-20 before administration to the animals.
2.3. Drugs and chemicals
The following chemicals and reagents were procured:
ranitidine (Martin Brown, Hisar, India), thiobarbituric acid
(Spectrochem, Mumbai, India), reduced glutathione (Hi-
media, Mumbai, India), 5,5’-dithionitrobenzoic acid (Hi-
media), bovine serum albumin (Hi-media), trichloroacetic
acid (TCA; Qualigens Fine Chemicals, Mumbai, India),
potassium chloride (Qualigens Fine Chemicals), sucrose
(Qualigens Fine Chemicals), EDTA (S.D. Fine-Chem, Mumbai,
India), sodium hydroxide (Spectrochem, Mumbai, India)
petroleum ether (40e60oC), ethanol, phenolphthalein (S.D.
Fine-Chem, Mumbai, India), phenol reagent (Ciocalteau-
Folins reagent; S.D. Fine-Chem, Mumbai, India), phenol
(Qualigens Fine Chemicals), sulfuric acid (Qualigens Fine
Chemicals), glucose (Qualigens Fine Chemicals), anhydrous
reagent (S.D. Fine-Chem), phenol red indicator, pyridine
(Spectrochem), n-butanol (Spectrochem), and Tris buffer
2.4. Phytochemical analysis
The ethanolic extract of the roots of A persica was sub-
jected to the following tests for phytochemical screening
using standard methods : carbohydrates were identified
by Molisch’s test, proteins were identified by the ninhydrin
test, triterpenoids and steroids by the Liebermann-Burchard
test, tannins by Braemer’s test, alkaloids by Dragendorff’s
test, saponins by the hemolytic test, glycosides by Legal’s
test, flavonoids by the Pew test, and fixed oils were iden-
tified by the presence of oil stains on filter paper .
2.5. Experimental design
The following groups were designed for this antiulcer study.
Each group was comprised of six animals.
? Group 1: vehicle (distilled water; DW)
? Group 2: DW þalcohol (control)
? Group 3: DW þ pylorus ligation (control)
? Group 4: DW þalcohol þranitidine (50 mg/kg)
? Group 5: DW þ pylorus ligation þranitidine (50 mg/kg)
? Group 6: DW þalcohol þethanolic extract (200 mg/kg)
? Group 7: DWþ pylorus ligation þethanolic extract
All animals were deprived of food (but not water) for
24 hours prior to being subjected to ulcerogenic compounds.
2.6. Alcohol-induced ulcer model
Gastric ulcers were induced by the oral administration of
absolute alcohol at a dose of 1 mL/200 g-body weight
45 minutes after the oral administration of the ethanolic
extract and identified drug to each group of animals .
Animals were sacrificed 1 hour after the administration of
ethanol. The stomachs were removed, cut along the
greater curvature, washed with normal saline (0.9%), and,
finally, and ulcer index was scored.
2.7. Pylorus ligation-induced ulcer model
This is the oldest animal model of gastric ulcers, originally
developed by Shay in 1945 . Wistar rats weighing
Antiulcer potential of Aerva persica merrill root81
150e200 g were fasted for 24 hours prior to pyloric ligation.
Under light ether anesthesia, the abdomen was opened by
a small midline incision below the xiphoid process, and the
pyloric position of the stomach was slightly lifted and
ligated to avoid traction into the pylorus or damage to its
blood supply. The stomach was carefully replaced and the
abdominal wall was closed by interrupted sutures. The
animals were deprived of both food and water the during
postoperative period and were sacrificed 6 hours after the
operation. The stomachs were dissected, and the contents
were drained into tubes and subjected to biochemical
analysis to determine the free acidity activity, pepsin
activity, and total carbohydrate and protein content .
The stomachs were then cut along the greater curvature,
the inner surface was examined for ulceration, and the
ulcer index was calculated.
2.8. Drug administration
The test drug (A persica at a dose of 200 mg/kg) and the
standard drug (50 mg/kg) were orally administered for 15
days to both ulcer models.
2.9. Measurement of the ulcer index
Ulcer scores were calculated viewing the ulcers with
a magnifying glass. The following bitrary scoring system was
used to grade the incidence and severity of the lesions :
? Shedding of epithelium Z 10
? Petechial and frank hemorrhagesZ 20
? One or two ulcersZ 30
? More than two ulcersZ 40
? Perforated ulcers Z50
UI ZUs þ Up ?10-1; where,
Us Z Mean severity of the ulcer score, and
Up Z Percentage of animals with ulcer incidence.
C - T/C ?100; where
C Zulcer index of the control group, and
T Z ulcer index of the treated group.
2.10. Biochemical parameters used to investigate
Determination of the dissolved mucosubstances was accom-
plished by determining the total carbohydrate and protein
in a 95% ethanol precipitate of the gastric juice. The total
carbohydrate and the total carbohydrate:protein (TC:PR)
ratio are acceptable as a reliable index of mucus secretion
and mucosal resistance . From the gastric juice, the
following parameters were determined: free acidity, pepsin
activity , total carbohydrate , and protein content
2.11. Estimation of free acidity
10 minutes. The volume of gastric juice was noted. One mL
gastric contentwas centrifugedat 1000 g
of the supernatant liquid was pipetted and diluted to 10 mL
with distilled water. Then, the total acidity of the gastric
juice was estimated by titration using 0.01 N sodium
hydroxide and phenolphthalein as the indicator. The result
was expressed as the free acid output, which was expressed
in terms of mEq/L .
2.12. Estimation of pepsin activity
The centrifuged (5000 g for 10 minutes) gastric juice
(0.1 mL) was added to 1 mL bovine albumin (0.5% w/v in
0.01 N HCl; pH 2) and incubated for 20 minutes at 37?C. A
duplicate background control tube (gastric juice blank), in
which 1 mL albumin was replaced with 1 mL of 0.01 N HCl,
was simultaneously run. Hydrolysis was stopped by adding
2 mL of 10% TCA. All of the tubes were heated in boiling
water for 5 minutes, then cooled. After denaturation of
the proteins by heating in a boiling water bath for
5 minutes, the precipitate was removed by centrifugation
(9000 g for 10 minutes). A total of 1 mL of the supernatant
was mixed with 0.4 mL of 2.5 N NaOH and 0.1 ml of the
Folin-Ciocalteu reagent, then the volume was adjusted to
10 mL using distilled water. Absorbance was measured at
700 nm. The peptic activity was calculated in terms of
micrograms of tyrosine liberated per milliliter of gastric
2.13. Estimation of the total carbohydrate content
blank was pipetted out into test tubes containing 0.15 ml
gastric juice or blank containing 0.15 mL of distilled water
and thoroughly mixed. Five mL of 96% H2SO4was added and
mixed slowly. After 10 minutes, the test tubes were shaken,
placed in water, and kept at 20?C for 20 minutes. The
optical density of the developed yellow-orange chromo-
phore was read at 482 nm using a UV spectrophotometer.
Several concentrations of a standard glucose solution were
run in order to prepare a standard curve. Total liberated
carbohydrates were expressed in terms of mg/mL-gastric
juice. The mucoadhesive activity was expressed as the
TC:PR ratio .
2.14. Estimation of the protein content
Estimation of the protein content was carried out as
described by Lowry . One mL of gastric juice and 9 mL
of 95% alcohol were mixed, shaken, and the mixture
centrifuged at 3000 g for 15 minutes in order to obtain the
precipitate. This precipitate was dissolved in 1 mL of 0.1 N
NaOH. Then, 0.9 mL of distilled water was added to 0.1 mL
of this solution. From this solution, 0.4 mL was placed in
another test tube. Four mL of an alkaline reagent was
added to this test tube and allowed to react for 10 minutes.
Then, 0.4 mL of the phenol reagent was added to this test
tube and allowed to react for 10 minutes until color
development. Readings were taken against the blank tubes
prepared with distilled water. The protein content was
obtained by comparing against a standard curve prepared
using bovine albumin. The protein concentrations were
expressed in terms of mg/mL-gastric juice ? Standard Error
82 N. Vasudeva et al.
2.15. Preparation of tissue homogenates
The rats were sacrificed by exsanguination through the
abdominal aorta while under light ether anesthesia. Four
hundred mg of muscle tissue was homogenized in 8 mL of
0.02 M EDTA in a Potter-Elvehjem homogenizer placed in an
ice bath. The homogenates were kept in the ice bath until
determination of the glutathione and malondialdehyde
2.16. Determination of the reduced glutathione
Five mL aliquots of the homogenates were mixed in 15 mL
test tubes with 4 mL distilled water and 1 mL of 50%
TCA. The tubes were intermittently shaken for 10e
15 minutes, then centrifuged for 15 minutes at 3000 rpm.
Two mL of the filtrate or supernatant was mixed with 4 mL
of 0.4 M Tris buffer (pH 8.9), 0.1 mL 5,5’-Dithio-Bis-(2-
Nitrobenzoic-Acid) (DTNB) was added, and the samples
were shaken. The absorbance was read within 5 minutes of
the addition of DTNB at 412 nm against a blank reagent
blank without a homogenate .
2.17. Determination of the malondialdehyde (MDA)
After washing the tissues with 0.9% NaCl, the homogenates
were prepared in a ratio of 1 g of wet tissue:9 mL of 1.15%
KCl using a glass Potter-Elvehjem homogenizer. The reac-
tion mixture contained 0.1 mL of the sample, 0.2 mL of
8.1% sodium dodecyl sulfate, 1.5 mL of 20% acetic acid
solution, and 1.5 mL of a 0.8% aqueous solution of thio-
barbituric acid (the pH of the 20% acetic acid solution was
adjusted with NaOH to be above 3). The mixtures were
finally adjusted to 4 mL with distilled water and heated at
95pC for 60 minutes. After cooling with tap water, 1 mL of
distilled water and 5 mL of the mixture of n-butanol and
pyridine (15:1, v/v) were added and the mixtures were
vigorously shaken. After centrifugation at 3000 rpm for
15 minutes, the absorbance of the organic layer (upper
layer) was measured at 532 nm .
2.18. Histopathological procedures
Tissue samples were preserved in 10% buffered formalin
and processed for paraffin block preparation. Sections
approximately 5-mm thick were cut using an optical rota-
tory microtome and stained with hematoxylin and eosin
. These sections were examined under a microscope for
2.19. Statistical analysis
All of the results are expressed as the mean ? SEM. The
data of all the groups were analyzed using one-way analysis
of variance (ANOVA) followed by the Dunnett’s t test using
Instat 3.0 (Graph Pad Software Inc., USA). In all of the tests,
the criterion for statistical significance was p< 0.05.
3. Results and discussion
3.1. Phytochemical analysis
Qualitative phytochemical analysis of the alcoholic extracts
of the root showed the presence of carbohydrates, flavo-
noids, saponins, alkaloids, and tannins. Flavonoids and
catechins are secondary metabolites that are present in
plants and have attracted the attention of many researchers
because of their wide range of biological activities .
Effect of A Persica extract on alcohol-induced ulcers.
Sr. No.TreatmentDose (mg/kg) Ulcer index* % Protection
Control (absolute alcohol)
1 mL/200 gm
34.60 ? 5.80
8.70 ? 2.80**
10.23 ? 2.30**
AP: Aerva Persica extract.
* The values of ulcer index are the mean ? SEM of the six animals in each group. Statistical analysis was performed using ANOVA
followed by Dunnett’s t-test.
** p<0.01 compared with control.
Effect of A persica extract on pylorus ligated-induced ulcers.
AP (200 mg/kg) 16.4 ? 3.0** 36.88
41.0 ? 4.3
189.5 ? 12.11 41.1? 3.6
117.6 ? 10.1** 27.76 ? 4.2*
82.3 ? 8.9**
523.6 ? 35.76
652.70 ? 21.43**
594.9 ? 18.45**
421.56 ? 44.78
316.18 ? 16.69* 2.06 ? 0.17**
377.78 ? 17.29** 1.57 ? 0.12**
1.24 ? 0.19
10.7 ? 2.1** 62.9513.8? 2.4**
AP: Aerva Persica extract.
***The values of the ulcer index are the mean ? SEM of the six animals in each group. Statistical analysis was performed using ANOVA
followed by Dunnett’s t test.
*p<0.05, **p<0.01 compared with the control.
Antiulcer potential of Aerva persica merrill root83
There are many studies on the antiulcerogenic properties of
flavonoids [20,21]. Tannins, saponins, and flavonoids are
known to affect the integrity of mucous membranes .
Tannins, with their protein precipitating and vasoconstric-
tive effects, prevent the development of ulcers. Flavonoids
are free radical scavengers that are known to play an
important role in ulcerative and erosive lesions of the
gastrointestinal tract . The antiulcer activities of the
ethanolic extract of this root could be attributed to its
flavonoids and tannins.
Qualitative phytochemical analysis of the ethanolic
extract of the roots of A persica.
*?/ þ indicates the absence or presence of the phyto-
3.2. Alcohol-induced ulcer model
Table 1 shows the ulcer index and percent protection from
ulcers in the alcohol-induced ulcer model. The extract
of the plant showed significant protection from ulcers
(70.43%) at a dose of 200 mg/kg (p< 0.01) compared with
the controls. The standard drug, ranitidine, also showed
a significant protective effect against ulcers (74.85%) at
a dose of 50 mg/kg when compared with the control groups
3.3. Pylorus ligation-induced ulcer model
The ulcer index and percent protection against ulcers in the
pylorus-induced ulcer model are shown in Table 2. The
extract of the plant showed significant protection against
ulcers (36.88%) at a dose of 200 mg/kg (p <0.01) when
compared with the control animals. The standard drug,
ranitidine, also showed significant protective effects
against ulcers (62.95%) at a dose of 50 mg/kg when
compared with the control groups (p <0.01). Free acidity
and pepsin activity were also significantly decreased at
a dose of 200 mg/kg of the extract, as shown in Table 2,
when compared with the control animals. The TC:PR
content ratios were significantly increased when compared
with the control groups.
The results indicate that the ethanolic extract of the
roots has potent protective effects against induced ulcers
in animal models. A significant decrease in the ulcer index
(p <0.01) was observed following treatment with the
Effect of the alcoholic extract of A persica on biochemical (i.e., antioxidant) parameters in rats.
ParametersControl Standard AP (200 mg/kg)
Malondialdehyde levels (nmol/mg of protein)
0.58 ? 0.03
78.00 ? 4.80
0.22 ? 0.07*
107.80 ? 1.70*
0.29 ? 0.03*
104.80 ? 8.10*
Results are the mean ? SEM.
*p<0.01 compared with the control.
AP: Aerva Persica extract.
showing its normal appearance. (B) Control group treated with
1 mL of absolute alcohol. (C) Control group 2: pylorus ligation-
induced ulcer. (D) Alcohol-induced ulcer: treated with 50 mg/
kg ranitidine. (E) Pylorus ligation-induced ulcer: treated with
50 mg/kg ranitidine. (F) Alcohol-induced ulcer: treated with
the extract of the root. (G) Pylorus ligation-induced ulcer:
treated with the ethanol extract of the root.
Histopathology of stomach. (A) Normal group
Sr. No. Phytoconstituents Ethanolic root extract*
84 N. Vasudeva et al.
ethanolic extract of the roots of A persica at dose of 200
mg/kg. The extract also significantly increased the glyco-
protein content of the mucosal cells, as seen by the
increase in the TC:PC ratio of the gastric mucosa.
4. Biochemical parameters
The alcoholic extract of the roots significantly reduced
malondialdehyde levels (p <0.01) and increased gluta-
thione levels in tissue homogenates (Table 3). Glutathione is
an important constituent of the intracellular protective
mechanism against a number of noxious stimuli, including
oxidative stress. Intracellular glutathione also seems to be
responsible for protecting gastric cell against ethanol-
induced injuries. The excessive generation of oxygen radi-
cals in the extracellular space and depletion of glutathione
in conjunction with the inhibition of glutathione peroxidase
activity are responsible for oxidative tissue damage of
the gastric mucosa after the administration of ethanol,
as suggested by various studies [24,25]. In our study,
decreased glutathione concentrations were observed in the
control groups, whereas the rats that were pretreated with
the ethanol extract of the root of A persica showed
a significant increase in the glutathione level, suggesting
that these extracts prevent the depletion of nonprotein
in the malondialdehyde level in the control rats is probably
due to the ability of ethanol to produce oxygen-free radi-
cals. Pretreatment with the extracts provided protective
effects to the mucosal membrane against ethanol.
4.1. Histopathological investigation
The histopathological investigation of the gastric mucosa
(Fig. 1) of the rats revealed that the ethanol treatment
caused hemorrhagic necrosis. Pretreatment with the
ethanol extract of the roots of A persica reduced ethanol-
induced hemorrhagic necrosis in the rat stomach in both
The results of our study indicate that the ethanolic extract
of A persica produces significant cytoprotective effects
against alcohol-and pylorus
(p< 0.01). Thus, the ethanolic extracts of A persica roots
can be used as a new source for antiulcer drugs.
Currently, non steroidal anti-inflammatory drugs (NSAIDs)
are commonly used as analgesics and anti-inflammatories,
which may cause ulcers. Various other factors, like alco-
holism, also cause ulcer. In these situations, we need drugs
that have less severe side effects and are highly potent. In
the light of these facts, the present study is highly relevant
and addresses the utility of the roots of A persica as an
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