Research Journal of Pharmacognosy and Phytochemistry.

7(2): April-June, 2015, 124-130

ISSN 0975-2331 (Print) www.anvpublication.org

0975-4385 (Online)

REVIEW ARTICLE
Antiulcer activity of natural compounds: A review
1 1 1 2
S. Prakash Rao *, Indu Amrit , Vijay Singh , Parag Jain
1
Columbia Institute of Pharmacy, Tekari, Raipur India-493111
2
Department of Pharmacology, Institute of Pharmaceutical Sciences,
Guru Ghasidas Vishwavidyalaya, Koni, Bilaspur India-495009
*Corresponding Author E-mail: spr_pharma@yahoo.co.in

ABSTRACT:
Peptic ulcer is a break in the lining of the stomach, first part of the small intestine, or duodenum. The duodenum
is the first part of the small intestine. Contrary to popular belief, ulcers are not caused by spicy food or stress but
instead are most commonly due to either an infection or long-term use of certain medications. The main goals for
treating a peptic ulcer include eliminating the underlying cause (particularly H. pylori infection or use of
NSAIDs), preventing further damage and complications, and reducing the risk of recurrence. Peptic ulcer which
is mainly caused by bacterial attack or excess of acid secretion can be cured effectively by these isolated plant
compounds. A number of drugs including proton pump inhibitors and H2 receptor antagonists are available for
the treatment of peptic ulcer, but clinical evaluation of these drugs has shown incidence of relapses, side effects,
and drug interactions. This has been the rationale for the development of new antiulcer drugs and the search for
novel molecules has been extended to herbal drugs that offer better protection and decreased relapse. Craving for
herbal medicines are still importance due lesser chance of adverse effects and easily available in surrounding
place with low cost. In this review attempts have been made to summarize medicinal plants and their
constituents used for peptic ulcer by the people of rural area which may be beneficial for the modern science.

KEYWORDS: Antiulcer, Isolated compounds, Alkaloids, flavonoids, Terpenoids.

INTRODUCTION:
A history of heartburn, gastroesophageal reflux disease Prevalence is higher in third world countries where it is
(GERD) and use of certain forms of medication can raise estimated at about 70% of the population, whereas
the suspicion for peptic ulcer. Medicines associated with developed countries show a maximum of 40% ratio.
peptic ulcer include NSAIDs (non-steroid anti-
inflammatory drugs) that inhibit cyclooxygenase, and Ulcers are an open sore of the skin or mucus membrane
most glucocorticoids (e.g. dexamethasone and characterized by sloughing of inflamed dead tissue. A
prednisolone). A major causative factor (60% of gastric gastric ulcer would give epigastric pain during the meal,
and up to 50-75% of duodenal ulcers) is chronic as gastric acid production is increased as food enters the
inflammation due to Helicobacter pylori that colonizes stomach. Symptoms of duodenal ulcers would initially
the antral mucosa. The immune system is unable to clear be relieved by a meal, as the pyloric sphincter closes to
the infection, despite the appearance of antibodies. Thus, concentrate the stomach contents; therefore acid is not
the bacterium can cause a chronic active gastritis (type B reaching the duodenum [2]. Peptic ulcer disease (PUD)
gastritis). Gastrin stimulates the production of gastric is an illness that affects a considerable number of people
acid by parietal cells. In H. pylori colonization responses worldwide. It develops when there is an imbalance
to increased gastrin, the increase in acid can contribute to between the ‘‘aggressive’’ and ‘‘protective’’ factors at
the erosion of the mucosa and therefore ulcer formation. the luminal surface of the epithelial cells. Aggressive
In Western countries the percentage of people with factors include Helicobacter pylori, HCl, pepsins,
Helicobacter pylori infections roughly matches age (i.e., nonsteroidal anti-inflammatory drugs (NSAIDs), bile
20% at age 20, 30% at age 30, 80% at age 80 etc.) [1]. acids, ischemia, hypoxia, smoking and alcohol. While
defensive factors include bicarbonate, mucus layer,
Received on 01.05.2015 Modified on 14.05.2015
mucosal blood flow, PGs and growth factors. [3]
Accepted on 28.05.2015 ©A&V Publications All right reserved
Res. J. Pharmacognosy & Phytochem. 7(2): April-June 2015; Page 124-130 Burning or gnawing feeling in the stomach area lasting
DOI: 10.5958/0975-4385.2015.00021.7

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between 30 minutes and 3 hours commonly accompanies controlled both by neuronal transmitters and blood-borne
ulcers [4]. mediators, as well as the chemistry of the stomach
contents. Amino acids and small peptides directly
In order to achieve this aim, various sources like ancient stimulate the gastrin-secreting cells.
traditional books, journals, libraries and internet were
explored for each of the medicinal plants for peptic Acetylcholine: Acetylcholine is released from (e.g.vagal)
ulcers and all retrieved articles were evaluated to achieve neurons and stimulates specific muscarinic receptors on
any in vitro, in vivo, or clinical evidence for their the surface of the parietal cells and on the surface of
efficacy and possible mechanisms. histamine-containing cells.

Etiology and Pathogenesis Histamine: Within the stomach, mast cells (or histamine-
Peptic ulcer occurs in that part of the gastrointestinal containing cells similar to mast cells) lying close to the
tract (GIT) which is exposed to gastric acid and pepsin parietal cell release a steady basal release of histamine,
i.e. the stomach and duodenum. The etiology of peptic which is further increased by gastrin and acetylcholine.
ulcer is not clearly known. It results probably due to an The hormone acts on parietal cell H2 receptors, which
imbalance between the aggressive (acid, pepsin, bile and are responsive to histamine concentrations that are below
Helicobacter pylori) and the defensive (gastric mucus the threshold required for vascular H2 receptor
and bicarbonate secretion, prostaglandins, nitric oxide, activation.
innate resistance of the mucosal cells) factors [5].
Prostaglandins: Prostaglandins (mainly E2 and I2),
A variety of psychosomatic, humoral and vascular synthesised in the gastric mucosa mainly by cyclo-
derangements have been implicated and importance of oxygenase-1, stimulate mucus and bicarbonate secretion,
Helicobacter pylori infection as a contributor to ulcer decrease acid secretion and cause vasodilatation, all of
formation and recurrence has been recognized [6]. which serve to protect the stomach against damage
(Figure-1).
In gastric ulcer; acid secretion is normal or low. In
duodenal ulcer; acid secretion is high in half of the Animal Models Used in the Screening of Antiulcer
patients but normal in the rest. Notwithstanding whether Activity
production of acid is normal or high, it does contribute to Various screening models are used for the screening of
ulceration as an aggressive factor, reduction of which is the anti ulcer activity it helps to understanding the
the main approach to ulcer treatment. etiology of the ulcer and screening of anti ulcer agents.

Regulation of Acid Secretion by Parietal Cells Cold restrain stress induced ulcer: Animal of different
The regulation of acid secretion by parietal cells is groups were subjected to cold stress after 45 min of the
especially important in the pathogenesis of peptic ulcer, formulation and OMZ treatment. Rats were deprived of
and constitutes a particular target for drug action. The food, but not water, for about 18 h before the
secretion of the parietal cells is an isotonic solution of experiment. Rats were immobilized by strapping the fore
HCl (150 m mol/l) with a pH less than 1, the and hind limbs in restraint cage and kept for 2 hr, at a
concentration of hydrogen ions being more than a temperature of 4°C. After 2 hr, animals were sacrificed,
million times higher than that of the plasma. The Cl-is the stomach was incised along the lesser curvature and
actively transported into canaliculi in the cells that ulcer was scored as: Red coloration (0.5), Spot ulcer (1),
communicate with the lumen of the gastric glands and hemorrhagic streak (1.5), Ulcers (2), Perforation (3).
thus with the stomach itself. This Cl- secretion is Mean ulcer score for each animal was expressed as ulcer
accompanied by K+, which is then exchanged for H+ index. The percentage of ulcer protection was calculated
from within the cell by a K+/H+ ATPase (+ and as- Mean ulcer index of control-mean ulcer index of test
bicarbonate ions [7]. The later exchanges across the / mean ulcer index of control x 100. [8]
basal membrane of the parietal cell for Cl-. The principal
stimuli acting on the parietal cells are: Aspirin induced ulcers: The above sections. After 45
min of formulations (6 ml/kg, p.o.) or ranitidine (50
Gastric: Gastrin is a peptide hormone synthesized in mg/kg, p.o.) treatment to different groups, the animals
endocrine cells of the mucosa of the gastric antrum and were administered with aspirin in dose of 500 mg/kg.
duodenum, and secreted into the portal blood. Its main The animals were sacrificed after 4 h and the stomach
action is stimulation of the secretion of acid by the was then excised and cut along the greater curvature,
parietal cells. Gastrin also indirectly increases rinsed gently with saline to remove the gastric contents
pepsinogen secretion, stimulates blood flow and and blood clots. Ulcer index was then calculated by
increases gastric motility. Release of this hormone is adding the total number of ulcers and calculate ulcer
index. [9]
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Figure 1-Formation of ulcer

Ethanol induced ulcer: The animals were divided into ulcers and centrifuged for 5 min at 2000 rpm. The
five groups as described above except that catechin (200 supernatant was collected and the volume of gastric juice
mg/kg, p.o.) was used as standard. The gastric ulcers was expressed as ml/100 g body weight. Total acidity
were induced in rats by administrating absolute ethanol was determined in the supernatant by titrating against
(99%) (1 ml/200 g) orally, after 45 min of formulations. 0.01 N NaOH, using 2-3 drops of topfers reagent as
They were kept in specially constructed cages to prevent indicator until canary yellow color was observed.
coprophagia during and after the experiment. The Volume of NaOH required was noted and this
animals were anaesthetized one hour later with corresponds to free acidity. Further 2-3 drops of
anesthetic ether and stomach was incised along the phenolphthalein was added and titrated with 0.01 N
greater curvature and ulceration was scored. The NaOH until pink color was restored and this gives total
percentage of ulcer protection was calculated as mean acidity. Free acidity and total acidity is expressed in
ulcer index of control-mean ulcer index of test / mean terms of 0.1 N HCL per 100 g of gastric contents. [11]
ulcer index of control x 100. [10]
Water immersion stress induced ulcers: Stress induced
Pylorus Ligation Induced Ulcer: After 1 hr of treatment ulcers were induced by force swimming in the glass
to different groups, the animals were anaesthetized using cylinder (height 45cm diameter 35cm) containing water
thiopentone sodium (35 mg/kg, i.p.), the abdomen was up to 35cm maintained at 35oc for 3 hrs. Animals were
opened and pylorus ligation was done without causing fasted 24 hrs prior to the experiment. After the drug
any damage in its blood supply. After 4 hr their treatment (standard/test) animals were allowed to swim
stomachs were dissected and its contents were collected for 3hrs then animal were dissected stomachs were
into tubes for analysis of volume of gastric juice, pH, removed. All stomachs were opened along the greater
total and free acidity. The ulcers were scored as curvature ulcer index and % inhibition was calculated
described under cold stress induced ulcers. The gastric and Histopathological studies conducted. [12]
juice was collected after 4 hr of Pylorus ligation induced
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Indomethacin induced ulcers: All the animals were was administered intraperitoneally after 30 min prior to
fasted 36 hours before administration of Indomethacin. the serotonin injection. The animals were sacrificed after
The animals were divided into groups. Each rat was 18 hr, their stomachs were removed and opened along
administered with the 20mg/kg Indomethacin orally.30 the greater curvature, and the ulcer index was
min prior to the administration of the Indomethacin determined. Percentage protection of the ulcers
standard/test drug was administered. The rats were calculated. Histopathological studies were conducted.
anaesthetized with ether 1 hour latter the stomach was [16]
incised through the greater curvature and examined for
the number of lesion under the dissecting microscope by Acetic acid induced ulcers: Rats were anaesthetized with
titrating with 0.01N NaOH using phenolphthalein as an pentobarbitone (35 mg/kg, ip). The abdomen was opened
indicator. gastric juice estimated for pepsin. Ulcer index and the stomach was visualized. A cylindrical glass tube
and % inhibition were calculated and histopathological (6 mm in diameter) was tightly placed upon the anterior
studies conducted for the stomach tissues. [13] serosal surface of the glandular portion of stomach 1 cm
away from the pyloric end. 50% acetic acid (0.06
Histamine induced ulcers: Guinea pigs weighing (300- ml/animal) was instilled into the tube and allowed to
400 gm) were divided into groups of six each and the remain for 60 sec on the gastric wall . After removal of
animals were fasted for 36 hours (water allowed) before acid solution, the abdomen was closed in two layers and
experiment. One ml of histamine acid phosphate (50 mg animals were caged and fed normally. Standard and test
base) was administered intraperitoneally. Promethazine drug administered orally 4 h after the application of
hydrochloride 5 mg was injected intraperitoneally 15 acetic acid and continued up to 9 days after induction of
min before and 15 min after histamine administration. ulcer. The animals were then sacrificed after 18 h of the
The standard/test drugs were administered by gavage 45 last dose of drug on 10th day of experiment to assess the
minutes before histamine. Four hours after ulcer size and healing. Ulcer index was calculated based
administration of histamine, the guinea pigs were upon the product of length and width (mm2/ rat) of
sacrificed by stunning. The anterior abdominal wall was ulcers. [17]
opened and the stomach dissected out. Stomach was
opened along the greater curvature ulcers were Hydrochloric acid induced ulcers: Rats weighing 150-
identified. Severity scores were calculated. 180gms are taken and they were divided into groups.
Histopathological studies were conducted on the Thirty minutes after the test or reference drug or the
stomach tissues. [14] control vehicle treatment, 0.6 M HCl was orally
administered to each rat. After 1 h the rats were
Reserpine induced ulcers: Adult albino rats weighing anaesthetised with excess of anaesthetic ether and
150-180gms were fasted for 24 hr. Animals were divided stomach was cut open along the greater curvature,
into different groups following water ad libitum. cleared of residual matter with saline and the inner
Reserpine (5mg/kg) administered intramuscularly rats. surface was examined for ulceration. Ulcer index and %
30 min after the administration of the standard or test ulcer protection. Histopathological were conducted by
drug or control vehicle (Distilled water) Gastric tissue samples from each group were fixed in
intraperitoneally. All the animals were sacrificed after 18 10% formalin for 24 h. The formalin fixed specimens are
hr, their stomachs were removed, opened along the embedded in paraffin and section (3-5μm) and stained
greater curvature and sum of lengths (mm) of all lesions with haematoxylin and eosin dye. The histochemical
for each rat was used as ulcer index and percentage sections are evaluated by light microscopy. [18]
protection of ulcers were calculated. Histopathological
studies were performed on the stomachs tissues. [15] Active Principles with Antiulcer Activity
Chemical constituents of plants are responsible for
Serotonin induced ulcers: Rats weighing 120-150gms various pharmacological activities. These constituents
were taken and they were randomly divided into groups. may be alkaloids, trepenoids, flavonoids, glycosides,
Animals kept fasting for 24hrs and water withdrawn 2hr terpens and resins. The list of biological sources
before the experiment. Serotonin creatinine sulphate provided which gives active compounds with antiulcer
(20mg/kg) was administered subcutaneously to rats. The activity (Table-1).
standard drug/test drug/ control vehicle (Distilled water)

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Table 1- Chemical Constituents from medicinal plants with Antiulcer Activity

S. No. Plants Name Chemical Constituents Family Effect Mode of Action Reference
1. Cucumis sativus 9-beta-methyl-19- (Cucurbitaceae) Active [78] Reduction in gastric 19
norlanosta-5-ene secretion [78]
(cucurbitane glycoside)
2. Alchornea Sulfhydryl (Euphorbiaceae) Active [79] Defensive mechanisms 20
glandulosa of the gastrointestinal
mucosa against
aggressive factors
3. Annona squamosa one 1-(4-β-D- (Annonaceae) Active [80] Inhibition of H(+) K(+)- 21
glucopyranosyloxyphen ATPase activity
yl)-2-(β-D-
glucopyranosyloxy)-
ethane (Ehtanone)
4. Tectona grandis Verbascoside (Verbenaceae) Active [81] Inhibition of H(+) K(+)- 22
(phenylethanoid) ATPase with
corresponding decrease
in plasma gastrin level
5. Sargassum Plastoquinones [82] Sargassaceae Active [82] Increase of PGE2 levels 23
micracanthum [82] [82]
6. Cinnamomum 3-(2-hydroxyphenyl)- (Fabaceae) Active [83] Inhibited the secretion of 24
cassia [83] propanoic acid [83] gastric acid [83]
7. Xenorhabdus Xenocoumacins Enterobacteriaceae Active [84] Inhibited the secretion of 25
nematophila [84] (metabolic product) [84 gastric acid [84]
8. Myracrodruon Tannin-enriched (Anacardiaceae) Active [85] Inhibited the secretion of 26
urundeuva Allemão fraction (TEF) [85] gastric acid [85]
[85]
9. Maytenus ilicifolia Heteroxylan (Celastraceae) Active [86] inhibited the secretion of 27
[86] (polysaccharides) [86] gastric acid [86]
10. Potent antiulcer l-serine [87] Active [87] Inhibit gastric secretion 28
Isolated product [87]
[87]
11. alpha-2 [1-(2,-dimethylphenyl)- Active [88] Due to activation of 29
adrenoceptor 3- alpha-2 adrenoceptors
agonist [88] isobutoxyamidinourea]h located presynapitcally
ydrochloride on the vagus [88]
(WHR1582A) [88]
12. Potent antiulcer 2-methyl-8- Active [89] Inhibits histamine- 30
Isolated product (phenylmethoxy)imidaz stimulated gastric
[89] ol[ 1,2-a ]pyridine-3- secretion [89]
acetonitrile[(SCH
28080) Imidazole [89]
13. Cochlospermum Arabinogalactans type II Cochlospermaceae Active [90]] Inhibition of Secretion of 31
tinctorium (poly-saccharides)[90] gastric juice and output
of acid and pepsin
activity [90]
14. Jasminum Methyl jasmonate (Oleaceae) Active [91] Reduction in gastric 32
grandiflorum [91] (volatile organic fluid volume, total
compounds) [91] acidity and an increase in
the pH of the gastric
fluid [91]
15. Alpinia galangal 1′S-1′-Acetoxychavicol (Zingiberaceae) Active [92] Increased the glutathione 33
[92] acetate [92] levels of gastric mucosa
and increase of PGE2
levels [92]
16. Aralia elata Araloside [93] Araliaceae) Active [93] Inhibition of Secretion of 34
[93] gastric juice [93]
17. Qualea grandiflora sitosterol [94] (Vochysiaceae) Active [94] PGE2 stimulate 35
[94] the secretion of
bicarbonate and mucus,
maintain mucosal blood
flow and regulate
mucosal cell turnover
and repair [94]

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18. Ammania baccifera Hentriacontane (Lytharaceae) Active [95] Increasing mucosal 36

[95] (alkane hydrocarbon) PGE2 content and by
[95] inhibiting histamine
secretion from mast cell
by inhibition of histidine
decorboxylase [95]
19. Aesculus Aescin[96] (Sapindaceae) Active [96] induced ulcer(rats) [96] 37
hippocastanum
L. [96]
20. Phyllanthus niruri 4-methoxy-securinine (Euphorbiaceae) Active [7] enhancing mucosal 38
L protection
possibly by mobilization
of endogenous prosta-
glandins [7]
21. Vinca minor Vincamine[9] . (Apocynaceae) Active[9] prostaglandin-mediated 39
L [9] mechanism [9]
22. Enantia chlorantha 7,8,-dihydro-8- (Annonaceae) Active[15] Enhanced mucus 40
hydroxypalmatine production [15]
(protoberberine-type
alkaloid) [15]
23. Melaleuca 3-hydroxyl-lup-20 (30)- (Myrtaceae) Active [58] Inhibition of gastric acid 41
bracteata F [58] ene-28-oic [58] [58]
24. Xylocarpus Photogedunin[67] (Meliaceae) Active[67] Inhibition of H(+) K(+)- 42
granatum [67] ATPase activity [67]

CONCLUSION: 12. Malairajan P, Geetha G, Narasimhan S, Jessi 2008. Evaluation of

anti ulcer activity of Polyalthia longifolia (Sonn) Thwaites in
This article provides a list of various isolated compounds experimental animals. Indian Journal of Pharmacology, 40(3),
used in the treatment of peptic ulcer with their chemical 126-128.
structure, experimental models and their mode of action. 13. Jhansirani M, Mohanalaxmi S, Sarvanakumar A. 2010.
An understanding of the mechanism and control of Evaluation of Anti-Ulcer Activity of Methanol Extract of
Dioscorea oppositifolia Tubers in Adult Wistar Rats.
gastric acid secretion of medicinal plants will elucidate International Journal of Preclinical and Pharmaceutical Research.
new pathway for research and treatment of peptic ulcer. 1(1),19-24.
14. Mohammad Arshad, Nagarajaiah BH, Kudagi BL 2012.
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