Acorus Calamus Linn.

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Evaluation of Gastric Ulcer Protective Activity of Acorus calamus Linn. in

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Medicinal Plants: Phytochemistry, Pharmacology and Therapeutics Vol. 4 | 455
23
Evaluation of Gastric Ulcer Protective
Activity of Acorus calamus Linn. in
Laboratory Animals
Chandana Choudhury Barua1*, Prakash Haloi1,
Suparna Sen1, Mousumi Hazarika1, Nayan Jyoti Hazarika1,
Debesh Chandra Pathak1, Achinta Gohain Barua1,
Ananta Madhab Barua1 and Iswar Chandra Barua1
ABSTRACT
Acorus calamus L. (Acoraceae) is an aromatic herb, indigenous to central Asia and Eastern
Europe. The plant is used in Ayurvedic medicine for treatment of various ailments, such as
epilepsy, headache, eye disorders, insomnia, loss of memory, ulcer etc. Each and every part of
the herb has potent medicinal property for which there is increasing popularity of the plant to
explore its multifarious pharmacological property. The root, rhizome extracts and aromatic
oil from the plant has been previously screened for its antioxidant potential. But whole plant
extract is yet to be screened for its possible bioactivity and antiulcer property. Therefore,
screening of anti-ulcer property of whole plant extract of Acorus calamus was chosen for the
study. In the present study, antiulcer activity of ethanolic extract of Acorus calamus L. was
studied using various antiulcer models viz. Indomethacin- induced, Hcl-Ethanol induced,
Pylorus ligation and water immersion stress models to assess the effect of classical purificatory
procedure on pharmacological action of Acorus calamus. Maximal effect of ethanolic extracts
showed at a dose of 200 mg/kg by reducing the ulcer score, ulcer index, gastric content and an
–––––––
1 Department of Pharmacology and Toxicology, College of Veterinary Science, Khanapara,
Guwahati – 2, Assam, India.
* Corresponding author: E-mail: chanacin@gmail.com
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456 | Medicinal Plants: Phytochemistry, Pharmacology and Therapeutics Vol. 4
increase in pH of gastric juice in all the ulcer models in rats compared with the control group
of animals. Based on the present study it can be inferred that the ethanol extract of Acorus
calamus might contain some phytochemical constituents against ulcer healing.
Keywords: Acorus calamus L., Anti ulcer activity, Indomethacin, Hcl-Ethanol, Pylorus ligation,
Water immersion.
Introduction
Ulcer is a condition, where there is erosion in the lining of the stomach or
duodenum and is caused by the disruptions of the gastric mucosal defense and
repair mechanism (Marslin et al., 2009). Gastric hyperacidity and ulcer are very
common, causing tremendous human suffering now a days. It is an imbalance between
damaging factors, within the lumen, and protective mechanisms within the gastro
duodenal mucosa. Although prolonged anxiety, emotional stress, hemorrhagic
surgical shock, burns and trauma are known to cause severe gastric irritation, the
mechanism, however, is still very poorly understood (Rao et al., 2000). Oxygen derived
free radicals implication, in the pathogenesis of a wide variety of clinical disorders
and gastric damage, caused by physical, chemical and psychological factors that
lead to gastric ulceration in human and experimental animals (Rao et al., 1999).
Although many products are used for the treatment of gastric ulcers e.g., antacids
and antihistaminics, most of these drugs, however, produce several adverse reactions,
like arrhythmias, impotence, gynecomastia and hematopoeitic changes (Ariypshi et
al., 1986).
There has been global resurgence of interest in herbal drugs in the recent past.
Though herbal medicines are effective in the treatment of various ailments, very often
these drugs are unscientifically exploited or improperly used. Therefore herbal drugs
deserve detailed studies in the light of modern medicine. A majority of population in
India suffer from hepatic and gastric ulcer disease due to various reasons. The modern
system of medicine still lack in providing suitable medicament for a large number of
diseases even though tremendous advances were made in the medicine. The
development of effective hepatoprotective and ulcer protective drugs were one of the
major thrust areas of research currently (Ethadi et al., 2013).
Plant extracts are some of the most attractive sources of new drugs, and have
been shown to produce promising results for the treatment of gastric ulcer (Pillai et
al., 1978). The precise biochemical changes during ulcer generation are not clear yet,
although various hypotheses have been proposed from time to time. Increased gastric
motility, vagal over activity (Cho et al., 1978), mast cell degranulation, low gastric
mucosal blood flow and decreased prostaglandin level (Miller, 1987) during stress
condition are thought to be the reasons of ulcer generation. Similarly role of oxygen-
derived free radicals have also been shown to play a role in experimental gastric
damage induced by ischemia and reperfusion (Perry et al., 1986), hemorrhagic shock
(Itoh et al., 1985) and ethanol administration (Mizui et al., 1986).
Acorus calamus Linn. (fam: Acoraceae) commonly known as Sweet flag, Sweet
Sedge, Myrtle Flag is a semiaquatic, perennial, aromatic herb with creeping rhizomes

originating in Asia but now widely distributed in Europe, North America and Africa.
It is also found indigenously in the marshy tracts of Kashmir, Shirmaur (Himachal
Pradesh), Manipur and in Naga Hills of India. The rhizome, root and leaf yield a
light brown to brownish yellow volatile aromatic oil known as calamus oil. The
alcoholic extract and the essential oil have been reported to possess in vitro
antimicrobial properties and antiulcer activity (Elaya et al., 2009). The alcoholic extract
of the plant is also reported to exhibit antiviral properties (Mamgain and Singh,
1994), insecticidal properties (Hasan et al., 2006). The rhizome is reported to be used
as an aromatic stimulant, an expectorant, a carminative, an anti-spasmodic, an emetic,
a laxative and a diuretic. Reportedly, an infusion of the rhizome is successfully used
in the treatment of dysentery, dyspepsia, intestinal worms, cough and fever (Dastur,
1951). Furthermore, the rhizome infusion is also used as a central nervous system
relaxant, a stomachic (Satyavati et al., 197), an appetite stimulant, an anthelmintic, a
vermifuge, an antibacterial agent, a sedative, an analgesic (Jain, 1968) and a
contraceptive (Malhi and Trivedi, 1972). Asarone has been reported to be the major
bioactive constituent of the volatile calamus oil. Isomeric forms of asarone commonly
found are a, b, of which a and b asarone are mostly responsible for the bioactivity of
Acorus calamus.
a-asarone has been reported to show anticarcinogenic properties (Parikh et al.,
1984). Traditional uses of this plant in NE India include use of fresh rhizome of the
plant against cold particularly in infants and also as a strong insect repellant. Rhizome
paste of the plant is applied on the body of the harvester of honey-sacs to get rid of
honey-bees. Protective effects of Acorus calamus on free radical scavengers and lipid
peroxidation in discrete regions of brain against noise stress exposed rat (Manikandan
et al., 2005) is reported. Pharmacological profile of Acorus calamus (Yende et al., 2009)
was also studied. Its blood pressure-lowering and vascular modulator effects of is
mediated through multiple pathways (Shah and Gilani, 2009). The antispasmodic
effect of Acorus calamus is mediated through calcium channel blockade (Gilani et al.,
2006). There are reports on the ethanol extract of Acorus calamus rhizomes on central
nervous system (Vohra et al., 1990). In vitro free radical scavenging activity of root and
rhizome extracts of Acorus calamus was reported (Elaya et al., 2010). In few instances,
cpSSR was successfully explored to know the diversity of Acorus calamus collected
from Northern India (Elaya et al., 2010). The present study was conducted with an
aim to investigate the ulceroprotective of the whole plant extract of Acorus calamus
along with phytochemical screening. Among all the solvents ethanolic fraction of the
plant was considered for our present study, since it has shown the best activity in the
preliminary study. The in vitro antioxidant potential of root and rhizome extracts of
Acorus calamus (Elaya et al., 2010) and the whole plant, Acorus calamus has been reported
by us (Barua et al., 2014).
Ulceroprotective analysis for the whole plant extract of Acorus calamus has not
yet been reported. Use of the whole plant as ulcer healing agent can be instrumental
in saving the plant from extinction by preservation of the root and rhizome of the
plant for further regeneration.

Materials and Methods

Preparation of Extracts
The plants were authenticated at the herbarium of Department of Agronomy,
Assam Agricultural University by Taxonomist Dr. I. C. Barua. For preparation of the
extracts, about 500gm of the powdered sample was dipped in sufficient amount of
ethanol (100 per cent for ethanolic) for several days in an air tight flask. Subsequently,
it was filtered and the filtrate was centrifuged. The supernatant was then transferred
to a rotary evaporator (Rotavapor R-210, Buchi) for removal of the solvent.
Phytochemical Analysis
The extracts were subjected to preliminary phytochemical screening to detect
the presence of different chemical groups of compounds such as steroids, phenolics,
tannins, flavonoids, glycosides, diterpenes, triterpenes and alkaloids (Harbome, 1991;
Bentley and Trimen, 1880; Khandelwal, 2009; and Kokate, 2000).
Animals
Male Wistar rats, weighing 180-250g, kept in controlled environment (temperature
22.2°C; humidity 60.4 per cent; natural light), maintained on a standard pellet diet
and water ad libitum were used. Such conditions were maintained for one week
before the experiments. The food was withdrawn 18-24 hour before the experiment,
though water was added ad libitum. All experiments were performed in the morning
according to current guidelines for the care of laboratory animals of IAEC (No.773/
03/ac/CPCSEA/FVSc, AAU/IEC/06/22).
Acute Toxicity Studies
The acute toxicity study of Ethanolic extract of Acorus calamus (EEAC) was
performed according to the Organization of Economic Corporation Development
(OECD) Guidelines No. 425. EEAC was administered orally at 2000 mg/kg to the
group of mice (n=3) and the percentage mortality, if any was recorded for a period of
24 hours. After the first hour of drug administration, the mice were observed for any
gross behavioral changes in the parameters like hyperactivity, grooming, convulsions,
sedation and loss of righting reflex, respiration, salivation and defecation (Vogel,
2002). The animals were fasted for 24 hours before oral administration of EEAC. The
control group received distilled water as vehicle. The animals were kept under
observation for the next 14 days. No mortality or gross abnormality was observed
with the given dose. Hence, based on the acute toxicity study, three oral doses viz.50,
100 and 200 mg/kg, were selected for anti ulcer activity study.
Anti-ulcer Activity
Indomethacin Induced Ulcer Model (Süleyman et al., 2001)
In this protocol, following overnight fasting, Indomethacin was administered
orally at 40mg/kg per os. After an hour, EEAC (50, 100 and 200 mg/kg) was
administered to the test rats, while omeprazole was given at a dose of 4 mg/kg p.o. to
the standard group, control group received distilled water. Five hours later, the animals

were euthanatized, the stomach and liver were removed for analysis of biochemical
parameters. The ulcer score and index were determined based on the extent of gastric
lesions. The pH and gastric volume were also determined.
HCl/ETH-Induced Ulcer Model (Hara and Okabe, 1985)
EEAC (50, 100 and 200 mg/kg) was administered orally to fasted rats, while
omeprazole (4 mg/kg) was given p.o to the standard group (positive control). The
control group (negative control) received distilled water. One hour after drug treatment,
1 ml of the necrotizing solution (150 Mm HCl in 60 per cent ethanol) was administered
to each rat. The rats were euthanatized after an hour; stomachs were opened along
the greater curvature and observed for ulcers in the glandular region. The gastric
content was measured (Nagar et al., 2012). The stomach and liver samples were
collected for biochemical analysis. The surface area of each lesion was measured and
scored for ulcer index using the formula (Hara and Okabe, 1985) [Ulcer index = 10/
X where X= total mucosal area/total ulcerated area]. Based on their intensity, ulcer
scores were given arbitrarily as, 0: Absence of any detectable lesion, 0.5: Small
Haemorrhagic effusion,1.0: Haemorrhagic effusion, 1.5: Mucosal ulceration of limited
diffusion involving more than 1/3 of the whole surface, 2.0: Mucosal ulceration of
limited diffusion involving more than 2/3 of the whole surface, 2.5: Mucosal ulceration
of generalized diffusion, 3.0: Deep ulcerations of limited diffusion, 3.5: Deep ulcerations
of generalized diffusion,4.0: Perforated ulcer.
Pylorus Ligation Induced Ulcer Model (Shay et al., 1945)
EEAC (50, 100 and 200 mg/kg) was administered orally to fasted rats, while
omeprazole (4 mg/kg) was given p.o to the standard group and control group received
distilled water, pyloric ligation was done by ligating the pyloric end of stomach of
rats of respective groups under ether anesthesia. Animals were allowed to recover
and stabilize in individual case and were deprived of water during post operative
surgery. After 4 h. of surgery, rats were sacrificed and ulcer score was calculated.
Gastric juice was collected and gastric secretions studied were performed.
Water Immersion Stress Model (Alphine and Word, 1999; Alder 1994)
Ulcer was induced by subjecting the animals fasted for 24 hours to swimming
for 4 hours by the method of Alphine and Word, (1969). The animals were sacrificed
after Four hours, ulcer score and ulcer index were determined followed by collection
of liver and stomach samples for analysis of biochemical parameters. The gastric
volume, pH, free and total acidity were also determined.
Collection of Gastric Juice
The gastric juice was collected and centrifuged for 1000 rpm for 10 minutes and
the volume of gastric juice was measured.
Biochemical Estimation of Antioxidant Enzymes
CAT, SOD, GSH and LPO assays were performed taking both liver and stomach
scrapings to study the effect of the extract on anti-oxidant enzymes in the organs. The
liver samples were prepared at a concentration of 200 g/L and the mucosal scrapings

were prepared at a concentration of 100 g/L in 20 mM Tris buffer (pH 7.4) and
centrifuged at 3000 g at 4°C for 30 min. The supernatant was collected to estimate
SOD (Marklund and Marklund, 1974), CAT (Aebi, 1984), GSH (Cohn and Lyle, 1966)
and LPO (Okhawa et al., 1979).
SOD (Superoxide Dismutase)
The spectroscopic assay for SOD (ECI,1.15 was performed by Marklund and
Marklund (1974) with slight modification and activity was expressed as units/mg
protein. Pyrogallol was used as a substrate and the rate of inhibition of pyrogallol
auto oxidation was taken from the increase in the absorbance at 540 nm UV-Vis
Spectrophotometer (Make Thermo Fischer Scientific Model 1119300).
Reduced Glutathione (GSH)
Reduced glutathione on reaction with DTNB (5,5’ dithiobis nitro benzoic acid)
produces a yellow coloured product that absorbs at 412 nm. Estimation was done by
using fluorometric method of Cohn and Lyle (1966). The absorbance was read at 412
nm within 5 minutes. Quantity of glutathione in the sample was calculated using
standard -glutathione and values represented as microg/mg protein
Catalase
Catalase activity was measured by the method of Aebi (1984). In the UV range,
hydrogen peroxide shows a continuous rise in absorption and decreasing wavelength.
The decomposition of hydrogen peroxide can be followed directly by the decrease in
extinction at 240 nm. The difference in extinction per unit time is a measure of catalase
activity. To 0.1 ml of sample, 2.9 ml of Phosphate buffer-H2O2 was added and the
absorbance was read for 3 minutes at 240 nm.
Lipid Peroxidation
Lipid peroxidation (LPO) was assayed according to the method of Okhawa et
al.,(1979). To 1ml of tissue homogenate, 1ml of normal saline (0.9 per cent w/v) and
2.0 ml of 10 per cent TCA were added and mixed well. The mixture (3000 g) was then
centrifuged at room temperature for 10 min to separate proteins. Then, 2 ml of
supernatant was taken and 0.5ml of 1.0 per cent TBA was added to it followed by
heating at 95°C for 60 min. to generate the pink colored MDA. OD of the samples was
measured at 532 nm. The levels of lipid peroxides were expressed as nM of MDA/mg
wet tissue using extinction co-efficient of 1.56 × 105 M-1 cm–1.
Histopathology
For histological studies, tissues were collected and fixed in 10 per cent neutral
formalin solution and dehydrated with a series of ethanol-xylene solutions. The
materials were processed by conventional paraffin embedding method. Microtome
sections were prepared at 6 µm thicknesses, mounted on glass slides, stained with
hematoxylin and eosin followed by observation for histopathological changes under
light microscope (Lee and Luna, 1968).

Statistical Analysis
Results were expressed as ±SEM (n=6). Statistical analysis were performed with
one way analysis of variance (ANNOVA) followed by Dunnett’s ‘t’ test P value less
than < 0.05 was considered to be statistically significant.*P>0.05, ** P>0.01 and
***P>0.001 when compared with the control group.
Results
Acute Toxicity Study
Mice did not show any gross abnormality up to a dose of 2000 mg/kg of EEAC,
based on which 50, 100 and 200 mg/kg doses were selected for different models of
anti-ulcer activity.
Indomethacin-Induced Ulcer Model
In indomethacin induced gastric ulcer model, the ulcer score, ulcer index, gastric
content were dose dependently reduced with elevation in gastric pH indicating ulcero
protective property of EEAC (Table 23.1). Elevation in the levels of GSH and CAT in
the stomach and liver samples and decline in SOD and LPO level in all the treated
and standard group when compared with the control group (Figure 23.1A).
CAT GSH
SOD LPO
Figure 23.1A: Indomethacin Induced Ulcer.

Table 23.1: Ulcer Protective Activity of Acorus calamus in different Ulcer Models in Wistar Rats
462 |
Models Groups Dose (mg/kg) Ulcer Score Ulcer Index Gastric Content (ml) pH
Indomethacin Control 10ml 2.95 ± 0.34 1.41 ± 0.17 6.84 ± 0.11 2.42 ± 0.25
Standard 4 0.31 ± 0.056*** 0.16 ± 0.01*** 1.57 ± 0.29*** 4.04± 0.21**
EEAC 200 0.25±0.063*** 0.09±0.02*** 2.25± 0.47*** 5.04±0.23***
EEAC 100 0.75±0.19*** 0.34±0.04*** 4.75±1.10*** 4.34± 0.45***
EEAC 50 2.3± 0.61 0.61±0.06*** 5.45± 0.67** 2.45± 0.67
Hcl-Ethanol Control 2.95 ± 0.17 1.41± 0.17 6.84 ± 0.11 2.42 ± 0.25
Standard 4 0.31 ± 0.03*** 0.16 ± 0.01*** 1.57 ± 0.29*** 4.04 ± 0.21**
EEAC 200 0.33± 0.03*** 0.16± 0.25*** 0.53±0.25*** 5.76±0.48***
EEAC 100 0.45± 0.05*** 0.34± 0.36*** 1.2±0.32*** 3.61± 0.74*
EEAC 50 0.51± 0.06*** 0.43± 0.45*** 1.34± 0.30*** 2.1± 0.39
Pylorus ligation Control 4.95 ± 0.17 4.41 ± 0.17 6.04 ± 0.11 2.12 ± 0.23
Standard 4 0.32 ± 0.03*** 0.36± 0.01*** 2.97 ± 0.27*** 5.04 ± 0.67***
EEAC 200 0.38± 0.08*** 0.27± 0.20*** 1.73±0.25*** 5.01±0.45***
EEAC 100 0.42± 0.04*** 0.39± 0.28*** 3.71±0.19*** 4.2 ± 0.67***

Water immersion Control 2.12 ±0.31 1.285± 0.32 2.5±0.35 1.95±0.38
Standard 4 0.05± 0.01*** 0.0045±0.002*** 0.2±0.045*** 5.3±0.18***
EEAC 200 0.145 ± 0.034*** 0.105±0.017*** 0.5±0.15*** 5.02±0.65***
EEAC 100 0.26 ± 0.041*** 0.155±0.036*** 1.5±0.35 3.65±0.56*
EEAC 50 0.365 ±0.037*** 0.301±0.035*** 1.9±0.42 2.34±0.23
EEAC- Ethanolic Extract of Acorus calamus.

Results were expressed as ±SEM (n=6). Statistical analysis were performed with one way analysis of variance (ANNOVA) followed by Dunnett’s ‘t’ test P
value less than < 0.05 was considered to be statistically significant.*P>0.05, ** P>0.01 and ***P>0.001 when we compared with the control group.
Medicinal Plants: Phytochemistry, Pharmacology and Therapeutics Vol. 4
HCl/ETH-Induced Ulcer Model

HCL/ETH induced ulcer model is a well-accepted model for the study of gastric
ulcer. In this model, EEAC 200 mg/kg dose showed significant reduction in gastric
content (p<0.001), acidity (p<0.001), ulcer score as well as ulcer index (p<0.001) as
compared to the control group (Table 23.1). However the standard drug, omeprazole
showed maximum protection in this model of ulcer. Enzymatic antioxidant
parameters such as SOD, CAT, and non-enzymatic GSH in the gastric stomach and
liver samples were increased in EEAC and omeprazole treated group as compared to
that of the control group. Subsequently, there was a decline level of LPO in a dose
dependent manner in EEAC treated groups and standard group.However, the
standard drug, omeprazole treated animals were superior to EEAC treated animals
in respect of ulcer protection (Figure 23.1B).
Pylorus-Ligation Ulcer Model
In pylorus –ligation ulcer model, reduction in the ulcer index, ulcer score and
gastric content and increase in pH were observed in EEAC and omeprazole treated
groups as compared to the control group (Table 23.1). Antioxidant enzymes like,
SOD, GSH and CAT levels were increased in comparison to the control group in
pylorus ligation induced ulceration in stomach and liver samples, while LPO level
decreased in EEAC when compared with control group (Figure 23.1C). In this ulcer
CAT GSH
SOD LPO
Figure 23.1B: Hcl/Eth Induced Ulcer Model.

CAT GSH
SOD LPO
Figure 23.1C: Pylorus Ligation Ulcer Model.
model also, standard drug, omeprazole was better than the extract treated group in
all the ulcer models.
Water Immersion Ulcer Model
The ulcer score, ulcer index, gastric content were dose dependently reduced
with elevation in gastric pH indicated ulcero protective property of EEAC in water
immersion induced ulcer. Antioxidant parameters such as SOD, CAT, and GSH in
the stomach and liver samples were increased in EEAC and omeprazole treated
group as compared to that of the control group and decline in LPO level in treated
and standard groups (Figure 23.1D).
Histopathological Study
In indomethacin induced ulcer model, necrosis of the mucosal epithelial cells of
gastric villi was observed in the control group (Figure 23.2A).. In the treated group
with 200 mg/kg dose of EEAC, the gastric mucosa showed necrosis and sloughing of
mucosal epithelial cells whereas, the standard treated group showed lesser necrosis
and sloughing of mucosal epithelial cell of the gastric mucosa (Figures 23.2B and C).

CAT GSH
SOD LPO
Figure 23.1(D): Water Immersion Stress Model.
Figure 23.1: Antioxidant parameters of liver samples in different models, representing

control, standard and EEAC treated groups. (A) Effect of EEAC on CAT, GSH, SOD and
LPO levels in Indomethacin –induced ulcer model (B) Effect of EEAC on CAT, GSH, SOD
and LPO levels in HCl/ETH- induced ulcer (C) Effect of EEAC on LPO levels on CAT, GSH,
SOD and LPO levels in Pylorus ligation induced ulcer model (D) Effect of EEAC on CAT,
GSH, SOD and LPO levels in Water immersion stress model.
In Hcl- Ethanol induced ulcer model, the control group showed necrosis of the
mucosal epithelial cell of gastric villi (Figure 23.2D). There was no visible histological
alternation in 200 mg/kg dose of EEAC and was found almost normal (Figure 23.2E).
In standard group, the erosion of gastric mucosa was observed (Figure 23.2F).
In Pylorus –ligation ulcer model, necrosis of the mucosal epithelial cells of gastric
villi was observed in control group, whereas the group treated with 200 mg/kg dose
of EEAC, the gastric mucosa did not show not much alteration except some focal
areas of necrosis of the villous epithelium (Figures 23.1G and H). The Standard
group showed massive necrosis and sloughing of the mucosal epithelial cells (Figure
23.2I).

Figure 23.2: Photomicrographs Showing Histological Changes in the Mucosal Tissue of

Stomach of Control, Standard and EEAC Treated Groups.
Indomethacin induced ulcer
(A) Control (10X)
Figure 23.2A: Indomethacin induced ulcer :Necrosis of the mucosal epithelial cells of
gastric villi in the control group.
(B) Standard (10X)
(C) 200 mg/kg (10X) dose
Figures 23.2B and C: In 200 mg/kg dose of EEAC, the gastric mucosa showed necrosis
and sloughing of mucosal epithelial cells; the standard treated group showed lesser
necrosis and sloughing of mucosal epithelial cell of the gastric mucosa.

HCL/ETH induced ulcer
(D) Control (10X)

Figure 23.2D: Hcl/Eth induced ulcer :The control group showed necrosis of the mucosal
epithelial cell of gastric villi.
(E) Standard (10X)
Figure 23.2E: No visible histological alternation (200 mg/kg dose of EEAC) and was found
almost normal.
(F) 200 mg/kg (10X) dose
Figure 23.2F: In pylorus ligation ulcer : In Standard group, the erosion of gastric mucosa,

Pylorus-ligation ulcer
(G) Control (10X)
(H) Standard (10X)
Figures 23.2G and H: Necrosis of the mucosal epithelial cells of gastric villi in control
group, in 200 mg/kg dose of EEAC, the gastric mucosa did not show not much alteration
except some focal areas of necrosis of the villous epithelium.
(I) 200 mg/kg (10X) dose

Figure 23.2I: The Standard group showed massive necrosis and sloughing of the mucosal
epithelial cells

Discussion
Gastric ulcer is defined as disruption of the mucosal integrity of the stomach
and/or duodenum leading to a local defect or excavation due to active inflammation.
Despite the constant attack on the gastro duodenal mucosa by a host of noxious
agents (acid, pepsin, bile acids, pancreatic enzymes, drugs, and bacteria), integrity is
maintained by an intricate system that provides mucosal defense and repair. Gastric
erosions and ulcers are induced by various factors including gastric over secretion
and retention, weakening and depleting agents of mucin layer, blood flow
disturbances, and mucosal injury and inflammation (Wallace et al., 1996; Neal, 2003;
Isobe et al., 2004; Byun et al., 2007). The ulcer inducing agents include non-steroidal
anti-inflammatory drugs (NSAID) that block production of prostaglandins, leading
to mucin depletion and blood flow disturbances (Slomiany et al., 1997; Filaretova et
al., 2002; Cao et al., 2004; Rao et al., 2004; Kim et al., 2005), alcohols (Cao et al., 2004;
Rao et al., 2004), stresses (Cao et al., 2004; Rao et al., 2004; Byun et al., 2007), leading to
gastric over secretion and retention (Rao et al., 2004; Cao et al., 2005), gastric hyper
motility and acetic acid accumulation (Dias et al., 2000; Rao et al., 2004; Cantarella et
al., 2005; Isbil et al., 2006; Cantarella et al., 2007), and Helicobacter pylori infection
(Wallace and Granger, 1996; Neal, 2003). For the therapy of gastric ulcers, proton
pump inhibitors that block acid secretion from parietal cells, antacids, histamine
receptor (H2) antagonists, prostaglandins that strengthen mucin layer and antibiotics
to eliminate Helicobacter pylori have been used (Wallace and Granger, 1996; Neal,
2003).
Stress plays an important role in the pathogenesis of ulcers by playing role in
number of factors like increase in gastric motility, vagal over activity (Cho et al., 1979)
mast cell degranulation (Cho et al., 1979) decrease gastric mucosal blood flow and
decrease prostaglandin synthesis (Millar et al., 1987). The role of acid is questionable
but decrease in mucous secretion has been reported during stress induced ulcer
(Guth et al., 1971). Stress causes both sympathetic and parasympathetic stimulation
of stomach leading to local hypoxia (near or actual “ischemia”). The ischemic condition
caused an increase in the levels H2O2 which in conjugation with O2 generates OH–
ions which oxidized various cellular constituents such as proteins, membrane lipids
and depletes glutathione. Lipid peroxidation causes loss of membrane fluidity and
loss of cellular function (Tandon et al., 2004).
Many natural products and modern synthetic drugs have been used to treat
gastric ulcer disease but so far, a complete cure has not been discovered and exploration
of new antiulcer drugs has remained a field of active research. (Amr-Ali, 1974). Several
medical products of natural origin were conceived in traditional systems of knowledge
and practice that has been transmitted over centuries and which continuously change.
In actual scenario, researchers of many countries involved in the modern drug
discovery processes are becoming increasingly aware of the value of their traditional
knowledge, while global pharmaceutical industry is looking for alternative solutions
to reduce the crescent innovation deficit and enhance the development of new
products.
Dengiz and Gursan,(2005) explained that the formation of ulcer induced by
indomethacin is caused due to the inhibition of cyclooxygenase action that prevents

prostaglandin biosynthesis which in turn inhibits the secretion of mucus, a preventive

measure of gastrointestinal tract. The involvement of neutrophil and its activation is
also a crucial factor in the indomethacin induced gastric damage (Verma et al., 2012).
EEAC conferred protection from indomethacin induced gastric ulcer in our study
indicating its ulcer protective property probably due to inhibition of cyclooxygenase,
which is however yet to be studied. The methanol extract of Oxalis corniculata revealed
the presence of alkaloids, saponin, phenolics, tannins and flavonoids in its
preliminary phytochemical screening and conferred gastroprotective activity by
reducing the ulcer score and ulcer index in indomethacin induced ulcer model (Sakat
et al., 2012). Thus, EEAC has a positive correlation between its phyto-constituents
and its ulceroprotective activity in indomethacin induced ulcer model in our study.
Over production of ROS contributes to pathobiological alterations in the mucosa.
The principle reacting oxygen metabolites altering the colonic milieu including SOD,
GSH and LPO (Abdolghaffari et al., 2010; Jagtap et al., 2011,). The superoxide anions
are transformed into secondary antioxidant H2O2 by SOD. GSH has a detoxifying
effect on electrophiles by direct reaction with various intermediates mediated by
GSH S-transferase. It is well studied that depletion of GSH leads to the cellular
damages. Depleted GSH is characteristic feature of colonic injury (Hagar et al., 2007).
Ethanolic extract of leaves of Moringa oleifera exhibited decrease in LPO level and
increase in SOD and CAT level with discontinuity in the lining of mucus epithelium
and/or no ulcer formation in cold stress restrain induced ulcer model in rat (Verma
et al., 2012). Thus, the results of EEAC implied that it has ability to restore the
antioxidant enzyme activities in this model.
Ethanol provoked gastric ulceration by a number of mechanisms that include
decrease in amount of gastric mucus and break down of the mucosal barrier, back
diffusion of acid, increased gastric mucosal permeability, leading to increase in
leakage of H+ from the lumen of gastrointestinal tract (GI), and decreased transluminal
electrical potential difference (Ramesh et al., 2011). Since ethanol causes damage in
gastric mucosa as well as in liver tissues, our study indicates that these damages
were reverted to normal after treatment. Ethanolic extract of Oxalis corniculata leaves
significantly increased SOD, CAT levels and percentage of protection and reduced
the ulcer index in ethanol induced ulcer model at 400 mg/kg dose (Patil et al., 2011).
Azadirachta indica bark extracts showed antiulcer activity in ethanol induced gastric
ulcer model in albino mice due to presence of flavonoids and phenolics compounds
(Recknagel and Ghoshal, 1966). Rats pretreated with J. sambac extract had reduced
submucosal edema and leukocyte infiltration along with reversal of liver and kidney
functions (Alrashdi et al., 2012). Hence, the results of EEAC showed a positive
correlation between mucosal ulcer parameters, mucosal tissue structure and its
phytochemical content in HCL/ETH induced ulcer model.
Pylorus ligation induced ulcers are due to auto digestion at the gastric mucosa
and the breakdown of the gastric mucosal barrier (Sairam et al., 2002). In case of
pyloric ligation, ulcer formation is mainly due to the stasis at the gastric juice and
stress (George et al., 1999). The anti secretory activity of the extracts was noticed in
pylorus ligation induced ulcer model. There was a decrease in gastric volume. Pyloric
ligation also causes increase in calcium level, which in turn is known to stimulate

free radical generation. Increase in calcium and free radicals are documented to
induce tissue injury and peptic ulcer. Moreover, induction of stress also generates
free radical, which causes mucosal damage and change in antioxidant enzymes
(Dias et al., 2000). The excess free radical generation causes various biochemical
changes, which was indicated by increases in the levels of TBARS, calcium, and LPO
activity but a decrease in the level of GSH. Mitochondria are able to store large amounts
of calcium and at the same time are the main sources of free radical generation in the
cell. These results suggest that inhibition of free radical generation is one of the
important contributing factors by which test extract showed its antiulcer property.
The present investigation provides pharmacological credence to the
ethnobotanical claims of Acorus calamus mentioned in the traditional Indian system
of medicine. However, fractionation of Acorus calamus needs to be carried out to
determine the isolated bioactive moieties responsible for healing effect of gastric ulcer
in laboratory animal.
Acknowledgements
The authors are grateful to Department of Biotechnology, (DBT), Govt of India,
New Delhi for financial assistance to conduct this research. Physical facility provided
by the Director of Research (Vety), Assam Agricultural University is also gratefully
acknowledged.
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Evaluation of Gastric Ulcer Protective Activity of Acorus calamus Linn. in

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Materials and Methods

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Figure 23.1A: Indomethacin Induced Ulcer.

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EEAC- Ethanolic Extract of Acorus calamus.

HCl/ETH-Induced Ulcer Model

Figure 23.1B: Hcl/Eth Induced Ulcer Model.

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Figure 23.1C: Pylorus Ligation Ulcer Model.

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Figure 23.1(D): Water Immersion Stress Model.

Figure 23.1: Antioxidant parameters of liver samples in different models, representing

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Figure 23.2: Photomicrographs Showing Histological Changes in the Mucosal Tissue of

(A) Control (10X)

(B) Standard (10X)

(C) 200 mg/kg (10X) dose

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HCL/ETH induced ulcer

(D) Control (10X)

(E) Standard (10X)

(F) 200 mg/kg (10X) dose

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(G) Control (10X)

(H) Standard (10X)

(I) 200 mg/kg (10X) dose

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prostaglandin biosynthesis which in turn inhibits the secretion of mucus, a preventive

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