Santhi Krupa et al. / Vol 10 / Issue 1 / 2020 / 1-6 .

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Pharmacological Screening
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www.ijpsmjournal.com Research Article

AN OVERVIEW ON A PERLICIOUS PEPTIC ULCER DISEASE AND

THE ANTIULCEROGENIC MEDICINAL PLANTS
D. Santhi Krupa1*, K. Padmalatha, T. Pooja Neelima1, K. Sireesha1, Sk. Sofiya Begum1, V.
Kusuma1, M. Sushma Reddy1
Department of Pharmacology, Vijaya Institute of Pharmaceutical Sciences for Women. Enikepadu, Vijayawada, Andhra
Pradesh, India.

ABSTRACT
Though the concept of gastric secretion, food digestion, acid in gastric juice, hyperacidity and gastric ulcers are known from
the 17th century, the treatment of peptic ulcer is still inappropriate. Some cases of gastric ulcer demand surgical approaches.
With medical advances, anti-secretory antiulcer and mucoprotective drugs are introduced. In the 19th century, with the
established H. Pylori mediated pathophysiology, it had demanded the inclusion of antibiotic therapy regimens. However, the
relapses, recurrences, side effects and more pronounced drug interactions of the drugs had widened the opportunity to explore
medicinal plants having antiulcer activity. This present review article will cover the etiology, pathology of peptic ulcer,
allopathic antiulcer drugs, their disadvantages and a view of antiulcer medicinal plants.

key words: Allopathic, recurrences, side effects, treatment, medicinal plants, microbial.

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DOI:
http://dx.doi.org/10.21276/ijpsm.2020.10.1.1

Received: 07.08.19 Revised:01.09.19 Accepted:24.09.19

INTRODUCTION or reoccurrence of existing drugs, as a gift of nature the

Peptic ulcer is an open sore that forms on an
epithelial surface and leads to loss of tissue lining the
lower esophagus, stomach, or duodenum. The incidence of
peptic ulcer disease (PUD) and its complications varies
across the world. Peptic ulcer disease can greatly impact
morbidity and mortality across the globe [1].
The perforated peptic ulcer was firstly quoted in case of
Princess Henrietta of England, 1620. In late 20 th century,
Barry Marshall and Robin Warren had identified H. pylori
as the microbial cause for peptic ulcers. Though the
disease was evident from ancient history, the treatment
part still demands the new leads to overcome the relapses
combinational therapy including medicinal plants to the
existing allopathic medicine can increase the safe and
effectiveness
of antiulcer treatment.
ETIOLOGY
The history of peptic ulceration sickness
ranges from resolution while intervention to the event
of complications like sore formation and perforation.
Hyperacidity, underneath production of mucosal
secretions, are the basis for the incidence of peptic
ulcer disease [8]. Apart from the acidity and mucus

Corresponding Author:-D. Santhi Krupa Email:-shanthikrupa@gmail.com

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factors, H.pylori will play a major role in gastric ulcer,
where as Campylobacter pyloridis, Cytomegalo virus,
Herpes simplex virus are aetiologically related to gastritis
mediated PUD. Zollinger-Ellison syndrome related
gastronoma’s secrete excessive levels of gastrin, the
pepsin and gastricsin precursors PGA (PGI) and PGC
(PGII), their activation will aggrevate acid secretion and
susceptibility to peptic ulcers [3,5]. Stress, smoking,
drinking alcohol or eating spicy food can worsen the
ulcers by initiating or delaying their healing. Aspirin,
indomethacin, phenylbutazone, clopidogrel,
bisphosphonates, spironolactone, glucocorticoids are the
Iatrogenic ulcer inducers [13]. Systemic mastoctosis,
myeloproliferative disease, vascular insufficiency,
radiation theraphy, crohns disease, sarcoidosis, hepatic
cirrhosis, renal failure and COPD are the other comorbid
factors.
PATHOPHYSIOLOGY
The basic pathology of peptic ulcer disease
involves an imbalance between aggravators like
hydrochloric acid, pepsin, ethanol, bile salts, NSAIDS and
defensors like mucus bicarbonate layer, prostaglandins,
mucosal blood flow, cellular regeneration. Excessive
gastric acid secretion and decreased mucosal defense are
the important factors, which in turn lead to the incidence
of PUD. The inhibition of endogenous prostaglandin
synthesis will decrease the defensors. Moreover, increased
histamine secretion, will subsequently increase the
secretion of acid or pepsin from parietal and gastric cells
[3].
Other valid microbial pathological factor is H.
Pylori that colonizes by attaching to the outer membrane
proteins of gastric epithelium further may cause changes
in WBC, plasma cells infiltration, releases pro-
inflammatory cytokines such as IL-1, IL-6, IL-8, and
TNF-α, which further initiates autoimmune gastric cell
apoptosis and tissue damage [10]. Production of different
enzymes urease, catalase and phospholipase can directly
or indirectly damage tissue. The method of H. pylori
transmission is unclear but seems to spread via a fecal-oral
route. The latrogenic NSAID-associated damage of the
gastroduodenal mucosa is the systemic inhibition of
constitutively expressed cyclooxygenase-1 (COX-1),
which is responsible for prostaglandin synthesis. The co-
administration of exogenous prostaglandins and
cyclooxygenase-2 (COX-2)-selective NSAIDs use reduces
mucosal damage and the risk of ulcers [1].
SYMPTOMS
Asymptomatic peptic ulcers are sometimes called
“silent ulcers.” The major symptom of a PUD is sharp,
intense, pulsatile epigastric pain, acid reflux or heartburn.
Others include upper fullness of stomach quickly after
eating, belching, or feeling bloated, nausea, in severe cases
vomiting and blood in the stools. The severity of the
symptoms depends on the intensity of gastric cell erosion.
DIAGNOSTIC TESTS
Peptic ulcer can be diagnosed by endoscopy or
other noninvasive tests. However, endoscopic tests are the
current gold standards. If an ulcer is detected, the doctor
may take a biopsy for examination. A biopsy can test
for H. pylori and look for evidence of any cancer. The
endoscopy may be repeated a few months later to
determine whether the ulcer is healing. Commercially
available nonendoscopic serologic tests are less reliable
and more expensive but can be used to rule out the
treatment. Rapid urease test can diagnose H.pyloric gastric
ulcers. Tests that can confirm a diagnosis include blood
and a breath test, using a radioactive carbon atom to
detect H. pylori or a stool antigen test to detect H. pylori in
the feces. Generally, semiquantitative enzyme-linked
immunosorbent assays are more accurate.
COMPLICATIONS
Although most peptic ulcers heal completely with
treatment, they can sometimes lead to complications. The
risk of serious complications depends on the cause, size,
location of the ulcer, the person’s age, dietary habbits and
the lifestyle. Major complications include bleeding,
perforation and gastric outlet obstruction. Bleeding ulcers
will affect older people, that can be treated by a proton
pump inhibitor or endoscopy involving cauterizing the
ulcer, by applying tiny clips to close off the blood vessels
followed by epinephrine, or using a special type of powder
to form a barrier. In rare cases, a person with a bleeding
ulcer may need surgery or embolization.
Perforation should be treated as quickly as possible.
Treatment usually involves the insertion of a nasogastric
tube, IV fluids, and medications. Gastric outlet
obstructions are treated by inserting a nasogastric tube to
remove food and fluid that has been unable to pass from
the stomach into the small intestine.
TREATMENT
Drugs that inhibit or neutralize gastric acid
secretion include proton pump inhibitors(PPI’s), histamine
H2-receptor antagonists, anticholinergics, prostaglandins
and, antacids.
Proton Pump Inhibitors (PPI’s)
Inhibition of the gastric H+/K+ -ATPase (proton pump)
enzyme system. The major disadvantage of proton pump
inhibitors is a concern for their long-term safety. These
drugs inactivate endocrine D cells and inhibit
somatostatin, which may result in hypergastrinemia. PPI’s
can affect the uptake of certain vitamins, minerals, and
medication, develops vitamin B12 deficiency, iron
deficiency anemia, reduce the antiplatelet action of
clopidogrel, since both are metabolized by the CYP2C19
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enzyme there will be decrease in ketoconazole absorption.
They might increase the risk for osteoporosis and bone
fractures by absorption of calcium salts. They facilitate the
absorption of digoxin suppression. Furthermore, PPIs can
affect the metabolism of other drugs metabolized by the
cytochrome (CYP) P450 system, they can delay the
clearance of warfarin, diazepam, and phenytoin(14).
H2 receptor blockers
The selective H2 blockers are less potent than the
proton pump inhibitors but, they will suppress 24 hour
gastric acid secretion by about 70%. Famotidine is the
most potent H2 antagonist available for clinical use, being
20-50 times more potent than cimetidine and 6-10 times
more potent than ranitidine [11].The H2 receptor blockers
are metabolized in the liver by the cytochrome P450
system and cause drug interactions.Lafutidine is a second
generation histamine H2 receptor antagonist the drug
activates calcitonin gene-related peptide, with resultant
stimulation of nitric oxide (NO) and regulation of gastric
mucosal blood flow. It also increases somatostatin levels
and increases mucin production by the gastric mucosa.
The high rates of ulcer recurrence following the
discontinuation of therapy like other antisecretory drugs
need continuous administration in.
Antacids
Antacids will increase gastric pH to greater than
fourand inhibits the proteolytic activity of pepsin.
Accumulation of individual ions is uncommon, but
aluminium encephalopathy may occur in the presence of
severe uraemia.
Anticholinergic drugs taken in doses that reduce
gastric acid secretion produce the expected side effects of
dry mouth, constipation, and urinary retention. Although
interference with the accommodation reflex can be
troublesome, the danger of precipitating acute glaucoma
has probably been overstated.
Cytoprotective/ Mucosal protectives
These agents such as organobismuth compounds
do not inhibit gastric acid secretion but reinforce the
mucus barrier include sucralfate and organic bismuth salts.
However, bismuth encephalopathy is a major toxicity
concern that needs to be addressed. drugs that. Sucralfate
is a complex salt of the sulfuric acid ester of sucrose) and
aluminium hydroxide which promotes mucosal repair
resulting in the healing of ulcers. Separation of aluminum
in the acid environment of the stomach forms a strongly
anionic species that binds to positively charged proteins
exuding from the ulcer forming a sticky paste. This binds
to the ulcer surface and protects it from the harmful effects
of acid, pepsin and bile. Sucralfate also utilizes its strong
negative charge to inactivate pepsin and bile [9]. This drug
also works against H. pylori.
Potassium-competitive acid blocker, rapid and
long acting vonoprazan vary from PPIs is that vonoprazan
inhibits the enzyme in a K+-competitive and reversible
manner, and does not require an acidic environment for
activation.
Apart from the above drugs, a highly potent
gastroprotective substance COX-2 analog (15-R-lipoxin
A4), nitric oxide releasing NSAIDs, protein therapy is the
novel changes in the antiulcer treatment.
Anti-H. Pyloric drugs
Though the primary focus was on symptomatic
treatment with anti-secretory agents, pathological evidence
of Helicobacter pylori (H. pylori) cases has directed
treatment towards the eradication of these bacteria.The
standard first-line Anti-H. pyloric therapy is a triple
therapy consisting of a proton pump inhibitor (PPI) and
two antibiotics, such as clarithromycin plus amoxicillin or
metronidazole given for seven to 14 days [5] or it can be
bismuth containing quadruple therapy for 14 days (PPI, a
bismuth salt, tetracycline, and metronidazole). Both
regimens yield eradication rates higher than 90%. Second-
line therapy is prescribed if a first-line regimen fails, and
includes Levofloxacin triple therapy (PPI, amoxicillin, and
levofloxacin) for 14 days seems to be an efficacious
therapy, achieving eradication rates between 74–81% [2].
Phytotherapeutics to treat peptic ulcer disease
The use of restorative plants in mending various
sicknesses is as old as people and surely understood as
phytotherapy. Moreover, in the past few years, there has
been a rising interest in alternative therapies and the usage
of herbal medicinal products [6]. Additionally, because of
the appearance of different side effects by utilization of
regular medications for various infections, therapeutic
plants are viewed as the significant store of medications.
Plant extracts and their crudes are the most huge
wellsprings of new medications, and have been appeared
to cause encouraging outcomes in the treatment of gastric
ulcer also [6]. The proton pump inhibitors,
anticholinergics, acid neutralizers, antibiotics, H2-receptor
blockers, sucralfate, and bismuth are not completely
compelling, and produce various antagonistic impacts, like
dryness of mouth, arrhythmia, hematopoietic adjustments,
hypersensitivity and gynecomastia [1, 7].
Moreover, the antiulcer drug clinical evaluation
had shown the incidence of relapses, side effects, and drug
interactions. Because of that, examinations of the new
pharmacologically dynamic specialists through the
screening of various plant phytochemical concentrates
prompted the revelation of compelling and safe
medications with gastroprotection. An indigenous drug
possessing fewer side effects is the major thrust area of the
present day research, aiming for a better and safer
approach for the management of PUD.
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Table 1. Antiulcer drugs, Category, MOA, Sideeffects

Category, Mechanisms
Proton Pump Inhibitors (PPIs)
Inhibition of the gastric H+/K+ -
ATPase (proton pump) enzyme
system
H2 Receptor Blockers
Blocking the action of histamine at Ranitidine
the histamine H2 receptors
Antacids
Increases gastric pH to greater than hydroxide
four, and inhibits the proteolytic
activity of pepsin
Cytoprotective Agents
Stimulate mucus production and
enhance blood flow throughout the
lining of the gastrointestinal tract
Potassium-Competitive Acid
Blocker
Inhibits H+ , K+ -ATPase in gastric
parietal cells at the final stage of
the acid secretory pathway
Drugs
Omeprazole, Lansoprazole
Rabeprazole, Esomeprazole
Pantoprazole
Cimetidine, Famotidine Nizatidine,
Aluminum hydroxide, Magnesium
Misoprostol, sucralfate
Vonoprazan
Side effects
Headache, Abdominal pain, Diarrhea,
Nausea, Vomiting Constipation, Flatulence,
Vitamin B12 deficiency, Osteoporosis
Headache, Anxiety, Depression Dizziness,
Cardiovascular events, Thrombocytopenia
Frequency not defined: Hypophosphatemia,
Chalky taste, Constipation, Abdominal
cramping, Diarrhea, Electrolyte imbalance,
Magnesium hydroxide Causes osmotic
retention of fluid
Constipation, Back pain, Cytoprotective
Agents, Misoprostol Stimulate mucus
production and enhance blood flow
throughout the lining of the gastrointestinal
tract, Diarrhea, Abdominal pain, Headache,
Constipation
Nasopharyngitis, Diarrhea, Upper respiratory
tract inflammation

Table 2. List of antiulcer medicinal plants

Biological Name Family Biological Name Family
Acacia arabica Mimosaceae Caesalpinia sappan Caesalpinieae
Adansonia digitata Malvaceae Capsicum annuum Solanaceae
Aegle marmelos Rutaceae Careya arborea Myrtaceae
Aframomum pruinosum Zingiberaceae Carica papaya Caricaceae
Allium sativum Liliaceae Cissus quadrangularis Vitaceae
Allophylus serratus Sapindaceae Cissus setosa Vitaceae
Aloe vera Liliaceae Cordia dichotoma Boraginaceae
Alstonia scholrs Apocyanacea Cyperus rotundus Cyperaceae
Anacardium accidentate Anacardiaceae Desmodium gangeticum Leguminosae
Annona squamosa Annonaceae Desmostachya bipinnata Gramineae
Archidendro njiringa Fabaceae Emblica officinalis Euphorbiaceae
Argemone mexicana Papaveraceae Eucalypus maculate Myrtaceae
Asparagus racemosus Asparagaceae Euphorbia neriifolia Eurphorbiaceae
Azadirachta indica Meliaceae Excoecaria agallocha Euphorbiaceae
Baccharis dracunculifolia Asteraceae Ficus religiosa Urticaceae
Baccharis trimera Asteraceae Galega purpurea Papilionaceae
Balsamodendron mukul Burseraceae Genista rumelica Fabaceae
Bauhinia variegate Caesalpiniaceae Glicyrriza glabra Fabaceae

Table.3. List of antiulcer medicinal plants

Biological Name Family Biological Name Family
Hemidesmusindicus Asclepiadaceae Peucedanumgrande Umbelliferae
Hibiscus rosasinensis Malvaceae Phyllanthus niruri Euphorbiaceae
Hieracium gymnocephalum Asteraceae Pinus longifolia Coniferae
Hydrocotylea siatica Umbelliferae Piper betel Piperaceae

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Indigofera tinctoria Papilionaceae Plantago ispagula Plantaginaceae

Ipomoea batatas Convolvulaceae Polyalthia longifolia Annonaceae
Ixorapa vetta Rubiaceae Psidiumguyava Myrtaceae
Kielmeyer acoriacea Guttiferae Rhizophora mangle Rhizophoraceae.
Kigelia Africana Bignoniaceae Rhuscoriaria Anacardiaceae
Lagenaria siceraria Cucurbitaceae Salvadora indica Salvadoraceae
Lawsonia alba Lythraceae Scutia buxifolia Rhamnaceae
Leucas lavandulifolia Labiatae Sesbania grandiflora Fabaceae
Mammea americana Calophyllaceae Shorea robusta Dipterocarpaceae
Mangifera indica Anacardiaceae Solanum nigrum Solanaceae
Maytenus robusta Celastraceae Solidago chilensis Asteraceae
Momordica charantia Cucurbitaceae Sylibin marium Asteraceae
Momordica cymbalaria Cucurbitaceae Syzygium aromaticum Myrtaceae
Morinda citrifolia Rubiaceae Tamarindus indica Caesalpiniaceae
Moringa oleifera Moringaceae Tanacetum larvatum Asteraceae
Morus alba Moraceae Tecomaria capensis Bignoniaceae
Morinda citrifolia Rubiaceae Terminali aarjuna Combretaceae
Myristicamalabarica Myristicaceae Terminalia chebula Combretaceae
Murrya koenigii Rutaceae Triticum aestivum Poaceae
Musa acuminata Lilaceae Utleria salicifolia Periplocaceae
Ocimum sanctum Lamiaceae Vernonia condensata Asteraceae
Odinawodier Anacardiaceae Vinca minor Apocynaceae
Oryzasativa Gramineae Zingibe rofficinalis Zingiberaceae
Osyrisquadripartita Santalaceae Utleria salicifolia Periplocaceae
Panax ginseng Araliaceae

CONCLUSION researcher to easily trace an ulcer protective or

This review summarises the focus on allopathic antiulcerogenic activity medicinal plant.
peptic ulcer drugs and the importance of the use of
medicinal plants either alone or in combination with other ACKNOWLEDGEMENT
allopathic drugs in ulcer prevention and ulcer healing. The None
list of evident antiulcer medicinal plants that are coated in
this article based on the literature review can help a CONFLICT OF INTEREST
None declared

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