Environmental Disease

: 2017  |  Volume : 2  |  Issue : 3  |  Page : 76--86

Pathophysiological status and nutritional therapy of peptic ulcer: An update

Mayank Kulshreshtha1, Gunja Srivastava2, Manjul Pratap Singh3,  
1 Depatment of Pharmacology, School of Pharmacy, Babu Banarasi Das University, Lucknow, Uttar Pradesh, India
2 Depatment of Pharmacognosy, School of Pharmacy, Babu Banarasi Das University, Lucknow, Uttar Pradesh, India
3 Depatment of Pharmaceutics, School of Pharmacy, Babu Banarasi Das University, Lucknow, Uttar Pradesh, India

Correspondence Address:
Mayank Kulshreshtha
School of Pharmacy, Babu Banarasi Das University, Faizabad Road, Chinhat, Lucknow - 226 028, Uttar Pradesh


Peptic ulcer (PU) is the most common disease of gastrointestinal tract (GIT) which affects the stomach and duodenum. It is characterized by an imbalance between the aggressive and defensive factors. Lifestyle and eating habits play an important role in the case of PU. According to the latest World Health Organization data published in April 2011, PU disease deaths in India reached 108,392 or 1.20% of the total deaths. The age-adjusted death rate is 12.37/100,000 of population, which leads India to 5th rank in the world. The aim of this review was to summarize the scientific data, herbal research, nutritional therapy, precautions, and pharmacological/nonpharmacological treatment regarding PU. The update conclusion regarding PU therapy was concluded with the help of published scientific data on Pub Med, Google Scholar, Med Know, Elsevier and other online resources. Natural remedies are found to be safe (minimum side effects) whereas, in allopathic treatment, antacids with the combination of proton pump inhibitors can better control PU. A balanced dietary plan should be advised by health care professionals or providers to patients suffering from PU. Following good habits and avoiding spicy food make our GIT healthy. Hence, a better lifestyle automatically cures the PU. Better knowledge with balanced lifestyle is an excellent treatment of PU.

How to cite this article:
Kulshreshtha M, Srivastava G, Singh MP. Pathophysiological status and nutritional therapy of peptic ulcer: An update.Environ Dis 2017;2:76-86

How to cite this URL:
Kulshreshtha M, Srivastava G, Singh MP. Pathophysiological status and nutritional therapy of peptic ulcer: An update. Environ Dis [serial online] 2017 [cited 2023 Mar 29 ];2:76-86
Available from: http://www.environmentmed.org/text.asp?2017/2/3/76/216533

Full Text


Peptic ulcer (PU) is a chronic development which is characterized by an imbalance between the factors (aggressive and defensive) that are harmful to the mucosa and its protection, finally occurrence of lesions on the lining of upper digestive tract.[1] The aggressive factors include acid, pepsin, nonsteroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori (H. pylori) whereas defensive factors include bicarbonates, mucus, mucus blood flow, and prostaglandins (PGs).[2] PU is also a group of disorders characterized by the presence of ulcers in any portion of gastrointestinal tract (GIT) exposed to acid in sufficient concentration and duration; such type of ulcerations most commonly occur in the stomach (gastric ulcer) or small intestine (duodenal ulcer [DU]).[3] Gastric ulcer is a deep lesion penetrating through the entire thickness of the GI mucosa and muscularis mucosa.[4] One of the theories was attributed to PU, to increase the acidity of gastric juices due to disturbances in vagal control.[5]

Perforation is one of the major complications in PU. The lifetime prevalence of perforation in patients with PU is about 5%. Perforation is often the first sign of PU disease. It is located in the lesser curvature of the stomach or on the anterior surface of the duodenum.[6],[7],[8],[9]

A study involving 84 patients suffering from perforated PU (PPU) reported severe epigastric pain (97.6%), abdominal distention (76.2%) and vomiting (36.9%). Abdominal tenderness and classical signs of peritonitis could be elicited in 88.1% and 66.7% of the patients, respectively, with PPU in this study. Other symptoms included nausea (35.7%), severe dyspepsia (33.3%), constipation (29.8%) and fever (21.4%). In our experience of managing 332 patients with PPU, the most common symptom was acute onset of abdominal pain (61.7%). A recent study in Taiwan has shown that patients with PPU were more likely to present to emergency room on weekends and this needs to be validated.[10],[11],[12]


The prevalence differs in the world population between the duodenal and gastric ulcers and the mean age of people with the disease is between 30 and 60 years, but it can happen in any age. Cosmopolitan difference has also been observed, and DUs are found to be rare in African people, but in the United States, the incidence is the same for all people. Regarding gender, there is a predominance of ulcers in males.[13] Approximately 500,000 persons develop PU in the United States each year. In 70% of patients, it occurs between the ages of 25 and 64 years.[14] The annual direct and indirect health-care costs of the disease are estimated at about $10 billion.[15] The differences in the prevalence of PU are existing in different parts of India,[16],[17],[18],[19] and PU is different from the disease in the West in being less acute and less likely to bleed or perforate.[20] On behalf of the clinical survey studied which has been done in North India, it has been concluded that PU and H. pylori haveoccurred frequently in this part of the country and PU was more prevalent in the elderly and dyspeptic patients. H. pylori was not concerned with dyspepsia and there was a low prevalence of PU in asymptomatic H. pylori-infected persons in this community. However, with an increase in elderly population in India, the number of PU patients is growing nowadays; the incidence of PU is increasing possibly as a result of unbalanced lifestyle, late to rise, alcohol and smoking, excessive intake of spicy food, personal hygiene etc.[21]

 Gastric Anatomy or Anatomy of Stomach

The stomach is the first intra-abdominal part of the GI or digestive tract. It is a muscular, highly vascular, bag-shaped organ that is distensible and may take varying shapes, depending on the build and posture of the person and the state of fullness of the organ.[22] The stomach lies in the left upper quadrant of the abdomen.[23] The stomach is a muscular, sac-like organ in the upper area of the abdomen. It is part of the digestive system. The stomach connects the esophagus to the duodenum, the first part of the small intestine. Since a meal can be eaten much more quickly than the intestines can digest and absorb it, one of the functions of the stomach is to serve as a mixing chamber and holding reservoir. At appropriate intervals after food is ingested, the stomach forces a small quantity of material into the first portion of the small intestine.[24] The stomach is divided into three regions: the fundus, the body and the antrum. At the distal end of the pyloric antrum is the pyloric sphincter, guarding the opening between the stomach and the duodenum. When the stomach is inactive, the pyloric sphincter is relaxed and open, and when the stomach contains food, the sphincter is closed.[25] Histologically, the stomach wall is divided into five layers. From superficial to deep, there is the serosa (peritoneum), the subserosa, muscularis externa, submucosa, and mucosa. The muscularis externa consists of an external longitudinal, a middle circular, and an inner oblique layer. The submucosa consists of loose connective tissue with large blood vessels. The mucosa lines the stomach cavity. It consists of an about 1-mm high single-layer columnar epithelium which is covered by a 100-200 μm thick mucus carpet. Further, gastric foveolae (at which ends the gastric glands sit) extend up to the muscularis mucosa. The tubular glands are formed by different exocrine cells which secrete various substances – depending on the part of the stomach.[26] Endoscopic ultrasonography (EUS) is a newer technical tool for evaluating stomach in the diagnosis and staging of early gastric cancer.[27],[28]

 Normal Physiology of Gastric Acid Secretion

Gastric acid secretion is a complex, continuous process in which multiple central and peripheral factors contribute to a common end point: the secretion of H + by parietal cells. Neuronal (acetylcholine), paracrine (histamine), and endocrine (gastrin) factors all regulate acid secretion. Their specific receptors (Acetylcholine, histamine and cholecystokinin B receptors respectively) are present on the basolateral membrane of parietal cells in the body and fundus of the stomach.[29] The regulation of acid and pepsin secretion reflects an intricate balance of chemo transmitters delivered to the gastric mucosa by several pathways that mediate both stimulatory and inhibitory mechanisms.[30] There are three phases in the secretion of gastric acid;[31] the cephalic phase: 30% of the total gastric acid to be produced is stimulated by anticipation of eating and the smell or taste of food.

The gastric phase: 60% of the acid secreted is stimulated by the distention of the stomach with food. The digestion produces proteins, which causes even more gastrin production. The intestinal phase: the remaining 10% of acid is secreted when chime enters the small intestine and is stimulated by small intestine distention.[32] Stomach secretes about 2.5 L of gastric juice daily. The primary exocrine secretions are pepsinogens, from the chief or peptic cells, and hydrochloric acid and intrinsic factor from the parietal or oxyntic cells.[33] Men secrete more acid than women. This can be explained partially by differences in body size.[34] Parietal cells have receptors for several stimulants of acid secretion and these cells possess a specific hydrogen potassium-ATPase enzyme (proton pump), which is responsible for the exchange of H + for K + ions across the apical surface of the parietal cells. The final process of acid transport per se rests with this enzyme. Three distinct but interdependent pathways deliver chemical messengers that stimulate acid secretion are controlled by the following pathway: the neurocrine pathway, which acts through the transmitters such as acetylcholine. The paracrine pathway delivers tissue factors, such as histamine from enterochromaffin-like cells. The endocrine pathway delivers hormones such as gastrin from antral G-cells.[35] The receptors on the surface of parietal cell include histamine receptor, responding to histamine released from specialized mast cells, receptors that are sensitive to the muscarinic effects of acetylcholine released from the vagus nerve, and probably receptors responsive to endogenouscirculating gastrin.[36] A stimulated receptor modifies the activity of other receptors and at the same time releases an intracellular second messenger. Calcium ions and cyclic AMP are the principal second messengers, and these in turn activate the gastric proton pump situated near the luminal apex of the parietal cell.[37]


The major observation regarding PU diseases is due to casual intake of NSAIDs, H. pylori infection and other factors which increase the level of acid and pepsin; as a result, they disrupt normal mucosal defense and healing mechanisms. Natural aggressors secreted into the gastric lumen are acid and pepsin. Various studies reveal that the gastroduodenal mucosal barrier is damaged by pepsin under conditions in which it is resistant to acid alone. Pepsin has mucolytic activity and progressively digests the adherent mucus layer at its luminal surface.[38]H. pylori infection plays a crucial role in the pathogenesis of PU disease. More than 95% of patients are suffering from DUs and about 70%–80% of patients with gastric ulcers are H. pylori positive.[39]H. pylori is a Gram-negative, motile, microaerophilic, curved bacillus that is found in the mucus layer overlying the gastric epithelium.[40] In 1981, Marshall and Warren conducted a prospective study of 100 consecutive patients undergoing endoscopy to correlate gastric mucosal biopsy findings with clinical and endoscopy data. In this investigation, they isolated microaerophilic, catalase-positive bacterium.[41]H. pylori infection has been recognized as the primary cause of chronic gastritis and PU disease.[42] In 1994, the United States National Institutes of Health Consensus Development Panel concluded that infection appears to play an important contributory role in the pathogenesis of PUs.[43] Antioxidant enzymes such as catalase, superoxide dismutase, and glutathione level involve in the pathogenesis of ulcer apart from the several factors such as tumor necrosis factor-α, reactive oxygen species, release of histamine, incidence of apoptosis, and bile acid secretion.[44],[45] PGs are capable of promoting inflammation and they also have protective role but sometimes inhibit stomach lining from the protective effect of acid. The NSAIDs block the functioning of COX family which is responsible for the production of PGs which protect the stomach lining.[46] Alcohol consumption also promotes ulcer; acid and gastrin level are increased by fermented alcohol. High dose of alcohol delays emptying and slows down bowel motility.[47] Other causes of ulcers can result in direct damage to the wall of the stomach or duodenum such as radiation therapy, burns, physical injury, smoking, stress, and lifestyle.[48],[49],[50] Some published researches indicate that the chances of H. pylori grown might be more in diabetic and obese patients with disturbed glucose function compared to normal people, and it was suggested that disturbance in glucose function may promote the H. pylori colonization due to changes in chemical level. Some other evidences explain that diabetic patients have low immune power so that they are more prone to H. pylori infection, but correlation between diabetes and H. pylori is not much more cleared.[51],[52],[53],[54],[55],[56]

 History of Peptic Ulcer

Indigestion and heartburn have been described for thousands of years, but it was only in the 16th century that the disease PU was established by autopsy. One of the first autopsy-proven pyloric PUs was studied in 1586 by Donatus of Mantua. Bauhin, in 1679, concluded that inflammation of the stomach led to a gastric ulcer which then ruptured. The first known gastric hemorrhage was reported in 1704.[57] The first classification of stomach diseases came in 1793 from Matthew Baillie, with clear descriptions of acute inflammation (arsenic), trichobezoar, ulcer, perforation, pyloric stenosis, scirrhous, and ulcerated cancer. In 1817, patients with perforated gastric ulcer were reported in Dublin by Crampton and patients with perforated DU were reported in London by Travers, who also noted bleeding, stenosing, and penetrating gastric ulcers.[58],[59],[60] The first epidemiological study on PU in North India was conducted in 1963.[61] Complications of PU disease including perforation, bleeding and obstruction, occur in up to 20% of cases; overall, gastric outlet obstruction may affect 5%–12% of PU patients.[62] Johnson and Ellis noted that PU disease was the origin of obstruction in 62% of patients from 1962 to 1975 and in 45% of patients from 1975 to 1985.[63] Gibson et al. investigated that only 33% of patients in their series with PU disease and outlet obstruction were H. pylori positive.[64] The annual incidence of gastric ulcers varies from approximately 1 case per 1000 population in Japan to 1.5 cases per 1000 population in Norway to 2.7 cases per 1000 population in Scotland.[65] Commonly, the ratio of DU to gastric ulcer varies with place and time. In most countries, DUs are about three times more common than gastric ulcers, but gastric ulcers are more common in some locations such as Japan, Sri Lanka, Andes and some islands of northern parts of Norway.[66]

 Miscellaneous Pathogenetic Factors and Nonpharmacologic Strategy for Ulcer Treatment

Cigarette smoking

Cigarette smoking has been implicated in the pathogenesis of PU disease (PUD). Not only have smokers been found to have ulcers more frequently than do nonsmokers, but also smoking appears to decrease healing rates, impairs response to therapy, and increases ulcer-related complications such as perforation. The mechanism responsible for increased ulcer diathesis in smokers is unknown. Some theories like altered gastric emptying, decreased proximal duodenal bicarbonate production, increased risk for H. pylori infection and cigarette-induced generation of noxious mucosal-free radicals play a important role in development of PU. Acid secretion is not abnormal in smokers. Despite these interesting theories, a unifying mechanism for cigarette-induced PU diathesis has not been established.[67],[68]

Emotional factor

Emotional disturbance due to stress in the pathogenesis of PU disease cannot be ignored.[69],[70] Emotional stress has been thought to contribute to PUD, but studies examining the role of psychological factors in its pathogenesis have generated conflicting results. Although PUD is associated with certain personality traits (neuroticism), these same traits are also present in individuals with nonulcer dyspepsia and other functional and organic disorders. Although more work in this area is needed, no typical PUD personality has been found. It has also been well reported that people who work in night shifts have a frequently higher incidence of ulcers than day workers.[71]

Role of other diseases

Ulcer may be associated with adenocarcinoma, signet ring carcinoma, leiomyosarcoma, lymphoma, and other neoplasms. Rarer causes of gastric ulcer include Crohn's disease (which manifests in the stomach or duodenum in [72]

Dietary factors

Various types of food stimulate mucosal defense factors in experimental models.[73] The incidence of PUD has decreased due to increase in the use of dietary essential fatty acids since the beginning of the 20th century.[74] Intake and handling of rice in various areas of the world may also explain peptic ulceration, as fresh rice oil in animal experiments protects against gastric ulceration, but stored oil is ulcerogenic.[75] Salt increases mortality from gastric ulcer but not DU.[76] Diet has also been thought to play a role in peptic diseases. Certain foods can cause dyspepsia, but no convincing studies indicate an association between ulcer formation and a specific diet. Alcohol is a known mucosal irritant; it causes marked irritation of the gastric mucosa. The only association between alcohol intake and ulcer disease exists in patients with portal cirrhosis. Coffee in both forms, regular and decaffeinated, contains peptides that stimulate the release of gastrin, a hormone that triggers the flow of gastric juice. Dietary fiber may be protective, as found in Swedish–Norwegian study, in which DUs relapsed more quickly on a low-fiber diet than on a bran-supplemented diet.[77] Milk, on the other hand, seems to have an adverse effect on the healing rate of DUs.[78] Duodenal ulceration is generally rare in areas of the world where the intake of dietary fiber in the form of unrefined wheat is the staple carbohydrate food eaten.[79] In 1978, Malhotra found that the rate of recurrence of duodenal ulceration was significantly lower in patients eating unrefined wheat compared to when they were on their previous more refined rice diet.[80] Consequently, both animal studies as well as studies in human beings show that a diet rich in fiber protects the GIT against the development of peptic ulceration.

 Uses of Nsaids

Decreasing the protective mucosal endogenous PGs and intestinal mucus, disrupting the intercellular junctions which lead to infiltration of enterobacteria, viruses and NSAIDs affects permeability and intestinal motility on gastroduodenal layers which result PU generation. Consequently, all these factors lead to penetration of bile acid, proteolytic enzymes, intestinal bacteria, and toxins causing epithelial cell damage and hence ulceration. Proton pump inhibitors (PPIs) increase heme oxygenase protein (HO-1) in the intestinal mucosa which is useful helpful in developing and proliferating the tissues.

It also inhibits inflammatory cytokines and neutrophil activation.[81] NSAID-induced ulcers develop in achlorhydric individuals, which has contributed to a widely held belief that acid is not involved in the pathogenesis of these lesions.[82] Thus, the prevention of NSAID-related gastropathy is an important clinical issue, and therapeutic strategies for both the primary and secondary prevention of adverse events are continually evolving.[83] Further reinforcing this hypothesis, there are several studies demonstrating that treatment with histamine H 2-receptor antagonists did not reduce the incidence of NSAID-induced ulceration.[84]


Probiotics are live microorganisms, which could interact with the GI upon administration.[85] They are widely used as functional foods, which have been advocated for the maintenance of GI microflora equilibrium and treatment of GI disorders.[86] Probiotics consist of Saccharomyces boulardii yeast or lactic acid bacteria, for example, Lactobacillus and Bifidobacterium species.[87] The importance of using protmics came from their abilities to eradicate H. pylori and their notable role in the exaggeration effect of multiple antibiotic regimens used for the H. pylori infection. The sulforaphane, an isothiocyanate abundant as its glucosinolate precursor present in certain varieties of broccoli and broccoli sprouts. This compound specifically is enriched in broccoli sprouts, inhibits extracellular, intracellular, and antibiotic-resistant strains of H. pylori and prevents benzopyrene-induced gastric tumors.[87],[88]

Genetic factors

Genetic predisposition has also been considered to play a role in ulcer development. First-degree relatives of DU patients are three times as likely to develop an ulcer; however, the potential role of H. pylori infection in contacts is a major consideration. Increased frequency of blood group “O” and the nonsecretor status have also been implicated as genetic risk factors for peptic diathesis. However, H. pylori preferentially binds to group “O” antigens. Therefore, the role of genetic predisposition in common PUD has not been established.[89]

Advanced age

Degeneration of pylorus permits bile reflux into the stomach, creating an environment that favors ulcer formation. Although there is no “antiulcer diet,” the patient should avoid foods and beverages (e.g., spicy foods, caffeine, and alcohol) that cause dyspepsia or that exacerbate ulcer symptoms.[90]

 Nutritional Care in Peptic Ulcer Disease

Calorie distribution for patients with PU should be normal, with values ranging from 50%–60% of carbohydrates, 10%–15% of proteins, and 25%–30% of lipids, with total energy value sufficient to maintain or recover the nutritional status.[91] Calorie distribution should be adjusted according to the patient's needs to normalize the nutritional status, having as recommended macronutrients a protein intake of up to 1.2 g/kg/weight/day in the acute stage of PU (5th–8th week) and up to 1.5 g/kg/weight/day in the recovery stage of PU.[92] To accelerate the healing process, in addition to protein, there are specific micronutrients such as zinc, which is essential to maintain the immune system function, as a response to oxidative stress, and to heal wounds.[93] Selenium may reduce infectious complications and improve healing.[94] In addition, Vitamin A may be used as a supplement, but research that supports this practice is of limited effectiveness, because very high dosages do not promote cure, and excessive intake may be toxic.[95] Today, milk is not recommended due to the buffering effect and the significant gastric acid secretion effect.[96]

Treatment strategies of peptic ulcer

Allopathic treatment of PU, pharmacology of antiulcer drugs, and home remedies for PU are listed in [Table 1], [Table 2], [Table 3] respectively.[97],[98]{Table 1}{Table 2}{Table 3}

 Other Approaches

According to the American College of Gastroenterology, therapeutic strategies for first-line treatment for H pylori infection are as follows:[99],[100]

Bismuth quadruple therapy (bismuth + PPI + tetracycline + nitroimidazole) for 10–14 days, especially for patients who are allergic to penicillinPPI + clarithromycin + amoxicillin + nitroimidazole for 10–14 daysPPI and amoxicillin, followed by 5–7 days with clarithromycin, a PPI and a nitroimidazole (conditional recommendation)7 days of a hybrid therapy with a PPI and amoxicillin, followed by 7 days with a PPI, amoxicillin, clarithromycin, and a nitroimidazole (conditional recommendation)10–14 days of levofloxacin triple therapy (levofloxacin, a PPI and amoxicillin) (conditional recommendation)(suggested option) 5–7 days of fluoroquinolone sequential therapy (a PPI and amoxicillin), followed by 5–7 days of a PPI, fluoroquinolone, and nitroimidazole (conditional recommendation)Endoscopy must be performed in patients aged >45-50 years and if the patients are associated with symptoms such as dysphagia, recurrent vomiting, weight loss and bleeding. Age is an independent risk factor for the incidence and mortality from bleeding PU, with the risk increasing in persons older than 65 years and increasing further in those older than 75 yearsA large international study demonstrated that, following successful endoscopic hemostasis for Forrest IB (oozing) PU bleeding, the risk of rebleeding at 72 h was very low (4.9%) compared with other stigmata of recent hemorrhage, but was similar to that for patients treated with esomeprazole (5.4%) and placebo (4.9%).[101]

 Precautions during Peptic Ulcer

Taking meal on time

It is very important for ulcer patients to take all meals on time and avoid snacking at odd times of the day between meals. Stomach acid is produced in response to food in order to digest it. Eating on time tunes the body into releasing the right amount of digestive juice at the right time. On the other hand, eating at odd times, such as between the meals, leads to overproduction of stomach acid. Therefore, ulcer patients are advised to take care of their meal timings and avoid cravings.[102]

Strictly avoid caffeine and alcohol

Caffeine is a popular stimulant found in a wide variety of food items. The highest content of the compound is found in tea, coffee, and chocolate. Patients with ulcer are advised to avoid taking caffeine since it aggravates pain in case of stomach ulcer. Excessive intake of this compound also causes acid reflux and heartburn, both of which are painful symptoms associated with the disease. Therefore, to prevent this extreme discomfort, ulcer patients should cut down their intake of food items and beverages which contain caffeine. At the onset of the disease, caffeine intake should be completely avoided for a couple of months. As the condition improves through medication, patients may enjoy a cup of coffee or tea in a day or small amounts of other food items containing caffeine. Individuals suffering from stomach ulcer should completely give up alcohol. It stimulates the production of acid in the stomach, thereby causing more damage to the stomach walls and increasing the associated pain. Alcohol may not cause any discomfort right away. However, patients mostly notice the effect around a day after the intake of alcohol. Therefore, it can lead to long-term damage unless ulcer patients completely give up their intake of alcoholic beverages. Stomach ulcer is caused when the walls of the stomach are damaged due to excessive production of acidic digestive juices. Individuals suffering from this condition experience multiple symptoms including abdominal pain, vomiting, indigestion, loss of appetite, and gradual weight loss. Although this damage is irreversible, the pain and associated discomfort can be alleviated through proper medication, a special diet, and certain precautions.[103]

Avoid hot spices

Although spicy food may not cause ulcers, it does aggravate the pain. Strong spices, such as red chilies, curry powder, mustard, and black pepper, should therefore be avoided. Hot, spicy meals can lead to acid reflux and indigestion which can be very painful for the sufferers of stomach ulcer. The condition can become worse despite ongoing treatment and medications. Therefore, it is advised to reduce the content of strong spices during the preparation of meals for the victims of this disease.[102]

Reduce salt intake

There is evidence that people with a H. pylori infection who have a high salt intake are at greater risk of developing stomach cancer. Try using seaweed instead of salt to provide flavor. Foods commonly high in sodium include canned soup, tortilla chips, potato/corn chips, salted nuts, salted meats (e.g., bacon), blue cheese, and cornflakes. There can also be a lot of hidden salt in soy sauce, pickled vegetables, some preserved or canned vegetables, packaged and processed foods, and preprepared meals. Read the labels and choose low-sodium varieties.[104]

Avoid chewing gum

The process of chewing food is known as mastication in scientific language. This process stimulates the production of gastric juices for the digestion of food as it passes down the alimentary canal. Chewing gum produces the same effect by leading to the production of stomach acid. However, since there is no food to digest, the acid damages the walls of the stomach. Therefore, the act of chewing gum can lead to the formation of ulcers and make the already existing condition worse. The patients of ulcer must avoid chewing gum, especially on an empty stomach when there is no food at all for digestion.[102]

Avoid fatty food

It is very important to maintain the overall health of the digestive system to avoid further complications in the case of stomach ulcer. Food items which stimulate the overproduction of digestive juice should be avoided. At the top of the list are fatty foods. In addition, food with a high content of simple sugars should also be avoided. Therefore, ulcer patients have to give up their love for junk food. Stay away from fried snacks, sugary delights, and fatty meals at all costs.[102]

Alleviate stress

Stress may not be a cause of the disease, but it has been linked to increased discomfort and pain. Individuals who face mental stress and excessive physical exertion in their daily life experience a slower healing time. Due to this reason, ulcer patients must find a way for reducing their level of stress. Practicing yoga, indulging in a good book, or spending quality time with family are just a few of the ways through which one can alleviate mental stress and get a break from the hectic day-to-day routine.[102]

Avoid milk

It has long been believed that milk helps in healing ulcer since it alleviates the associated pain. However, milk soothes the pain only for the time being as it coats the lining of the digestive tract. In fact, it leads to more damage and pain since it stimulates the secretion of digestive juices. Ulcer patients should not, therefore, turn to a glass of milk to relieve their pain.[102]

Follow the right dietary plan

A specific stomach ulcer diet and precautions can help patients fight the pain and discomfort effectively. Have a look at the following discussion to know about the right foods which can help in healing and alleviating painful symptoms of stomach ulcer. Antioxidants such as Vitamin C and β-carotene also help in the protection of the lining of the stomach and intestine. Foods high in these antioxidants include carrots, cabbage, apples, and kiwi fruit. However, avoid citrus fruits despite their high Vitamin C content since they are high in acid which can cause more pain and discomfort. Vitamin E promotes the healing of the damaged lining of the digestive tract and helps in treating stomach ulcer. Food substances with a high content of Vitamin E include avocado, hazelnut, sunflower seed oil, and wheat germ. An intake of high fiber diet promotes the formation of mucin. The layer of mucin protects the walls of the digestive tract against acid damage. Therefore, eating fruits, vegetables, and whole-meal bread and cereals will help heal stomach ulcers. Turn to a healthy source of protein, such as tofu, legumes, beans, and poultry, with the layers of fat and skin removed. Protein will help in maintaining the overall health of ulcer patients who have to eliminate quite a large number of food items from their dietary plan.[102]

Herbal treatment for peptic ulcer

There are plenty of plants which have antiulcer property as listed in [Table 4].[105],[106],[107],[108],[109],[110],[111],[112],[113],[114],[115],[116],[117],[118]{Table 4}


India ranked 5th worldwide in age-adjusted death rate due to PU. There are several treatment strategies to treat PU, but herbal-based cure may exhibit better option than synthetic one. Natural/herbal medicines provide a favorable environment in the management, treatment, or healing of PU. The application of natural things in daily food can easily control PU such as vitamins. It can be concluded that, by controlling causes that improving the lifestyle, food habits etc and inclusion of herbal plants or herbs in daily diet may reduce the occurrence of disease which in turn decreases the death rate due to PU.


I would like to express my hearty thanks to Dr. Manjul Pratap Singh, Sr. Assistant Professor, School of Pharmacy, BBD University, Lucknow, for gave me research oriented advises, as a guide always promote me for my better future and made this paper possible.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Nieto BY. Therapeutic protocol of peptic ulcer. Med 2012;11:179-82.
2Bennet PN, Brown MJ. Clinical Pharmacology. 9th ed. New Delhi: Churchill Livingstone Publication; 2006. p. 625-32.
3Helms RA, Herfindal ET, Quan DJ, Gourley DR. Peptic ulcer disease and gastroesophageal reflux disease. In: Text Book of Therapeutics Drug and Disease Management. 8th ed. Philadelphia: Lippincott Williams and Wilkin Publication; 2006. p. 1227-56.
4Tarnawski A, Szabo IL, Husain SS, Soreghan B. Regeneration of gastric mucosa during ulcer healing is triggered by growth factors and signal transduction pathways. J Physiol Paris 2001;95:337-44.
5Avram M. Peptic ulcer disease. Surg Clin North Am 1976;56:1277-84.
6Bas G, Eryilmaz R, Okan I, Sahin M. Risk factors of morbidity and mortality in patients with perforated peptic ulcer. Acta Chir Belg 2008;108:424-7.
7Vaira D, Menegatti M, Miglioli M. What is the role of Helicobacter pylori in complicated ulcer disease? Gastroenterology 1997;113:S78-84.
8Dongo AE, Uhunmwagho O, Kesieme EB, Eluehike SU, Alufohai EF. A five-year review of perforated peptic ulcer disease in Irrua, Nigeria. Int Sch Res Notices 2017;2017:8375398.
9Williams N, Bullstrode C, Connell PO. Stomach and duodenum. In: Bailey and Love's Short Practice of Surgery. 26th ed. London UK: CRC; 2013.
10Chalya PL, Mabula JB, Koy M, Mchembe MD, Jaka HM, Kabangila R, et al. Clinical profile and outcome of surgical treatment of perforated peptic ulcers in Northwestern Tanzania: A tertiary hospital experience. World J Emerg Surg 2011;6:31.
11Anbalakan K, Chua D, Pandya GJ, Shelat VG. Five year experience in management of perforated peptic ulcer and validation of common mortality risk prediction models – Are existing models sufficient? A retrospective cohort study. Int J Surg 2015;14:38-44.
12Kao LT, Tsai MC, Lin HC, Pai F, Lee CZ. Weekly pattern of emergency room admissions for peptic ulcers: A population-based study. World J Gastroenterol 2015;21:3344-50.
13Martins LC, Corvelo TC, Oti HT, Barile KA. Helicobacter pylori empacientes com úlcera gástrica na região Norte do Brasil. Med Trop 2002;35:307-10.
14Sonnenberg A, Everhart JE. The prevalence of self-reported peptic ulcer in the United States. Am J Public Health 1996;86:200-5.
15Available from: http://www.cme.med.umich.edu/pdf/guideline/PUD05.pdf. [Last accessed on 2012 May 07].
16Somervell TH, Orr IM. Some contributions to the causation, pathology and treatment of duodenal ulcer and its complications. Br J Surg 1936;24:227-45.
17Dogra JR. Studies on peptic ulcer in South India. Indian J Med Res 1940;28:145-61.
18Hadley GG. Studies of peptic ulcer as found in South India. Indian Council of Medical Research Reports 1959;39:31-3.
19Malhotra SL, Majumdar CT, Bardoloi PC. Peptic ulcer in Assam. Gut 1964;5:355-8.
20Raghavachari C. Note on peptic ulcer. Ind Coun Med Res 1959;39:48-51.
21Gregg LA. Note on peptic ulcer. Indian Council of Medical Research Reports 1959;39:65-7.
22Singh V, Trikha B, Nain CK, Singh K, Vaiphei K. Epidemiology of Helicobacter pylori and peptic ulcer in India. J Gastroenterol Hepatol 2002;17:659-65.
23Agur AM, Lee MJ, Grant JC. Grant's Atlas of Anatomy. 10th ed. London: Lippincott Williams and Wilkins; 1999.
24Gray H, Lewis WH. Gray's Anatomy of the Human Body. 20th ed. New York: Bartleb; 2000.
25Tortora G, Derrickson B. Principles of Anatomy and Physiology. 12th ed. United State of America: John Walley & Sons; 2009.
26Anne W. Ross & Wilson Anatomy and Physiology in Health and Illness. 12th ed. Canada: Elsevier; 2014.
27Available from: https://www.kenhub.com/en/library/anatomy/the-stomach. [Last accessed on 2017 May 10].
28Grant JC, Basmajian JV, Slonecker CE. Method of Anatomy: A Clinical Problem-Solving Approach. 11th ed. London, UK: Williams and Wilkins; 1989.
29Romanes GJ. Thorax and Abdomen. Cunningham's Manual of Practical Anatomy. 15th ed. New York: Medical Publications, Oxford University Press; 1986.
30Hoogerwerf WA, Pasricha PJ. Agents used for control of gastric acidity and treatment of peptic ulcer and gastric esophageal reflux disease. In: Hardman JG, Limbird LE, editors. Goodman & Gillman the Pharmacological Basis of Therapeutics. New York: McGraw-Hill; 2001.
31Schubert ML, Peura DA. Control of gastric acid secretion in health and disease. Gastroenterology 2008;134:1842-60.
32Lloyd KC, Debas HT. Peripheral regulation of gastric acid secretion. In: Johnson LR, Christensen J, Jackson MJ, editors. Physiology of the Gastrointestinal Tract. New York: Raven Press; 1994.
33Beradi RR, Welage LS. Peptic ulcer disease. In: Dipirio JT, Tolbert RL, Yee GC, Matzke GR, Wells BG, Posey LB, editors. Pharmacotherapy a Pathophysiologic Approach. 7th ed. New York: McGraw Hill Medical; 2007.
34Rang HP, Dale MM, Ritter JM, Moore PK. Diseases of the stomach and duodenum. In: Pharmacology. 5th ed. Philadelphia: Churchill Livingstone Publication; 2003.
35Richardson CT. Role of aggressive factors in the pathogenesis of peptic ulcer disease. Scand J Gastroenterol Suppl 1990;174:37-43.
36Satoskar RS, Bhandarkar SD, Ainapure SS. Pharmacotherapy of peptic ulcer disease. In: Pharmacology and Pharmacotherapeutics. 18th ed. Mumbai: Popular Prakashan; 2013.
37Tasman-Jones C. Pathogenesis of peptic ulcer disease and gastritis: Importance of aggressive and cytoprotective factors. Scand J Gastroenterol Suppl 1986;122:1-5.
38Allen A, Pearson JP, Blackburn A, Coan RM, Hutton DA, Mall AS, et al. Pepsins and the mucus barrier in peptic ulcer disease. Scand J Gastroenterol Suppl 1988;146:50-7.
39Metzger J, Styger S, Sieber C, von Flüe M, Vogelbach P, Harder F, et al. Prevalence of Helicobacter pylori infection in peptic ulcer perforations. Swiss Med Wkly 2001;131:99-103.
40Lee DH, Park HJ, Song SY, Lee SJ, Choi W, Lee YC, et al. Evaluation of therapeutic regimens for the treatment of Helicobacter pylori infection. Yonsei Med J 1996;37:270-7.
41Cello JP. Helicobacter pylori and peptic ulcer disease. Am J Roentgenol 1995;164:283-6.
42Matsukura N, Onda M, Yamashita K. Helicobacter pylori in peptic ulcer and gastric cancer. Gan To Kagaku Ryoho 1995;22:169-78.
43Mahendran P, Vanisree AJ, Shyamala Devi CS. The antiulcer activity of Garcinia cambogia extract against indomethacin-induced gastric ulcer in rats. Phytother Res 2002;16:80-3.
44Srivastava DP, Rajani GP, Gupta N, Sharma RK, Mandal S. Antiulcer and anti-inflammatory activity of fresh leaves of Polyalthia longifolia in rats. Int J Drug Dev 2011;3:351-9.
45Vella V. Drug induced peptic ulcer disease. MCPP 2005;10:15-9.
46Bujanda L. The effects of alcohol consumption upon the gastrointestinal tract. Am J Gastroenterol 2000;95:3374-82.
47Graham DY, Rakel RE, Fendrick AM, Go MF, Marshall BJ, Peura DA, et al. Recognizing peptic ulcer disease. Keys to clinical and laboratory diagnosis. Postgrad Med 1999;105:113-6, 121-3, 127-8.
48Han KS. The effect of an integrated stress management program on the psychologic and physiologic stress reactions of peptic ulcer in Korea. J Holist Nurs 2002;20:61-80.
49Jarosz M, Dzieniszewski J, Dabrowska-Ufniarz E, Wartanowicz M, Ziemlanski S, Reed PI, et al. Effects of high dose Vitamin C treatment on Helicobacter pylori infection and total Vitamin C concentration in gastric juice. Eur J Cancer Prev 1998;7:449-54.
50Kang JY, Yeoh KG, Chia HP, Lee HP, Chia YW, Guan R, et al. Chili – Protective factor against peptic ulcer? Dig Dis Sci 1995;40:576-9.
51Donath MY, Shoelson SE. Type 2 diabetes as an inflammatory disease. Nat Rev Immunol 2011;11:98-107.
52Devrajani BR, Shah SZ, Soomro AA, Devrajani T. Type 2 diabetes mellitus: A risk factor for Helicobacter pylori infection: A hospital based case-control study. Int J Diabetes Dev Ctries 2010;30:22-6.
53Bener A, Micallef R, Afifi M, Derbala M, Al-Mulla HM, Usmani MA, et al. Association between type 2 diabetes mellitus and Helicobacter pylori infection. Turk J Gastroenterol 2007;18:225-9.
54Gulcelik NE, Kaya E, Demirbas B, Culha C, Koc G, Ozkaya M, et al. Helicobacter pylori prevalence in diabetic patients and its relationship with dyspepsia and autonomic neuropathy. J Endocrinol Invest 2005;28:214-7.
55Anastasios R, Goritsas C, Papamihail C, Trigidou R, Garzonis P, Ferti A, et al. Helicobacter pylori infection in diabetic patients: Prevalence and endoscopic findings. Eur J Intern Med 2002;13:376.
56Ko GT, Chan FK, Chan WB, Sung JJ, Tsoi CL, To KF, et al. Helicobacter pylori infection in Chinese subjects with type 2 diabetes. Endocr Res 2001;27:171-7.
57Baron JH. Peptic ulcer. Mt Sinai J Med 2000;67:58-62.
58Baillie M. The Morbid Anatomy of Some of the Most Important Parts of Human Body. London: J. Johnshon, St. Paul's Church yard and G. Nicol, Pall Mall; 1793.
59Crampton J. Rupture of the stomach and escape of its contents into the cavity of the abdomen. Med Chir Trans 1817;8:228-31.
60Travers B. Additional observations. Med Chir Trans 1817;8:231-45.
61Sharma MP, Ahuja V. Current management of acid peptic disorders. J Indian Acad Clin Med 2003;4:228-33.
62Barksdale AR, Schwartz RW. The evolving management of gastric outlet obstruction from peptic ulcer disease. Curr Surg 2002;59:404-9.
63Johnson CD, Ellis H. Gastric outlet obstruction now predicts malignancy. Br J Surg 1990;77:1023-4.
64Gibson JB, Behrman SW, Fabian TC, Britt LG. Gastric outlet obstruction resulting from peptic ulcer disease requiring surgical intervention is infrequently associated with Helicobacter pylori infection. J Am Coll Surg 2000;191:32-7.
65Shrestha S, Lau D. Gastric Ulcers. Available from: http://www.emedicine.medscape.com/article/175765-overview. [Last accessed on 2009 Oct 12].
66Calam J. Clinical science of Helicobacter pylori infection: Ulcers and NSAIDs. Br Med Bull 1998;54:55-62.
67Available from: http://www.ptolemy.ca/members/archives/2007/ulcer/docs/dempsey.pdf. [Last accessed on 2009 Oct 13].
68Lam SK, Lee NW, Koo J, Hui WM, Fok KH, Ng M, et al. Randomised crossover trial of tripotassium dicitrato bismuthate versus high dose cimetidine for duodenal ulcers resistant to standard dose of cimetidine. Gut 1984;25:703-6.
69Bleich A, Ratan Y. Possible relationship between psychological stress and bleeding erosive upper gastrointestinal lesions. Harefuah 1996;131:7-9, 72, 71.
70Sullivan RM, Gratton A. Lateralized effects of medial prefrontal cortex lesions on neuroendocrine and autonomic stress responses in rats. J Neurosci 1999;19:2834-40.
71Available from: http://www.umm.edu/patiented/articles/what_causes_peptic_ulcers_000019_2.htm. [Last accessed on 2017 May 10].
72Available from: http://www.clinicaladvisor.com/gastroenterology-hepatology/peptic-ulcer-disease/article/596514/. [Last accessed on 2017 May 10].
73Glise H. Epidemiology in peptic ulcer disease. Current status and future aspects. Scand J Gastroenterol Suppl 1990;175:13-8.
74Hollander D, Tarnawski A. Dietary essential fatty acids and the decline in peptic ulcer disease – A hypothesis. Gut 1986;27:239-42.
75Jayaraj AP, Rees KR, Tovey FI, White JS. A molecular basis of peptic ulceration due to diet. Br J Exp Pathol 1986;67:149-55.
76Sonnenberg A. Dietary salt and gastric ulcer. Gut 1986;27:1138-42.
77Rydning A, Berstad A, Aadland E, Odegaard B. Prophylactic effect of dietary fibre in duodenal ulcer disease. Lancet 1982;2:736-9.
78Kumar N, Kumar A, Broor SL, Vij JO, Anand BS. Effect of milk on patients with duodenal ulcers. Br Med J (Clin Res Ed) 1986;293:666.
79Rydning A, Berstad A. Dietary aspects of peptic ulcer disease. Scand J Gastroenterol Suppl 1985;110:29-33.
80Malhotra SL. A comparison of unrefined wheat and rice diets in the management of duodenal ulcer. Postgrad Med J 1978;54:6-9.
81Bjarnason I, Hayllar J, MacPherson AJ, Russell AS. Side effects of nonsteroidal anti-inflammatory drugs on the small and large intestine in humans. Gastroenterology 1993;104:1832-47.
82Wallace JL, Muscará MN. Selective cyclo-oxygenase-2 inhibitors: Cardiovascular and gastrointestinal toxicity. Dig Liver Dis 2001;33 Suppl 2:S21-8.
83Schlansky B, Hwang JH. Prevention of nonsteroidal anti-inflammatory drug-induced gastropathy. J Gastroenterol 2009;44 Suppl 19:44-52.
84Agrawal NM. Epidemiology and prevention of non-steroidal anti-inflammatory drug effects in the gastrointestinal tract. Br J Rheumatol 1995;34 Suppl 1:5-10.
85Brzozowski T, Konturek PC, Mierzwa M, Drozdowicz D, Bielanski W, Kwiecien S, et al. Effect of probiotics and triple eradication therapy on the cyclooxygenase (COX)-2 expression, apoptosis, and functional gastric mucosal impairment in Helicobacter pylori-infected Mongolian gerbils. Helicobacter 2006;11:10-20.
86Lam EK, Yu L, Wong HP, Wu WK, Shin VY, Tai EK, et al. Probiotic Lactobacillus rhamnosus GG enhances gastric ulcer healing in rats. Eur J Pharmacol 2007;565:171-9.
87Williams NT. Probiotics. Am J Health Syst Pharm 2010;67:449-58.
88Fahey JW, Haristoy X, Dolan PM, Kensler TW, Scholtus I, Stephenson KK, et al. Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo[a] pyrene-induced stomach tumors. Proc Natl Acad Sci U S A 2002;99:7610-5.
89Penner R, Fedorak RN, Madsen KL. Probiotics and nutraceuticals: Non-medicinal treatments of gastrointestinal diseases. Curr Opin Pharmacol 2005;5:596-603.
90Available from: https://www.hopkinsmedicine.org/gastroenterology_hepatology/_pdfs/esophagus_stomach/peptic_ulcer_disease.pdf/Advanced/age/reference. [Last accessed on 2017 May 10].
91Kenneth R, Quaid M. Drugs used in the treatment gastrointestinal disease. In: Kat Jung BG, editor. Basic and Clinical Pharmacology. 10th ed. New York: McGraw-Hill; 2000. p. 1009-11.
92Marotta K, Floch MH. Diet and nutrition in ulcer disease. Med Clin North Am 1993;77:88-17.
93Reis NT. Nutrição Clínica: Sistema Digestório. 1st ed. Rio de Janeiro: Rubio; 2003.
94Prasad AS. Zinc: Role in immunity, oxidative stress and chronic inflammation. Curr Opin Clin Nutr Metab Care 2009;12:646-52.
95Ferguson M, Cook A, Rimmasch H, Bender S, Voss A. Pressure ulcer management: The importance of nutrition. Medsurg Nurs 2000;9:163-75.
96Arnold M, Barbul A. Nutrition and wound healing. Plast Reconstr Surg 2006;117:42S-58S.
97Tripathi KD. Drug for Peptic Ulcers, Essential of Medical Pharmacology. New Delhi: Jaypee Brother's Medical Publishers; 2009.
98Available from: http://www.healthline.com/health/natural-home-remedies-ulcers#cranberry7. [Last accessed on 2017 May 10].
99Chey WD, Leontiadis GI, Howden CW, Moss SF. ACG clinical guideline: Treatment of Helicobacter pylori infection. Am J Gastroenterol 2017;112:212-39.
100Zullo A, Hassan C, Campo SM, Morini S. Bleeding peptic ulcer in the elderly: Risk factors and prevention strategies. Drugs Aging 2007;24:815-28.
101Jensen DM, Eklund S, Persson T, Ahlbom H, Stuart R, Barkun AN, et al. Reassessment of rebleeding risk of Forrest IB (Oozing) peptic ulcer bleeding in a large international randomized trial. Am J Gastroenterol 2017;112:441-6.
102Available from: http://www.organsofthebody.com/stomach/stomach-ulcer-diet-and-precautions.php. [Last assessed on 2017 May 11].
103Available from: http://www.frantzmd.info/Expert%20 Patients/Peptic%20Ulcers.htm. [Last assessed on 2017 May 11].
104Available from: https://www.napiers.net/stomach-ulcer-diet.html. [Last assessed on 2017 May 11].
105Nadkarni AK. Indian Materia Medica. 3rd ed. Mumbai: Popular Prakashan; 1976.
106Abd El-Mawla AM, Osman HE. Effects of Gum acacia aqueous extract on the histology of the intestine and enzymes of both the intestine and the pancreas of albino rats treated with Meloxicam. Pharmacognosy Res 2011;3:114-21.
107Srivastava S, Jaiswal J, Gautam H, Sharma S, Rao CH. Anti-ulcer activity of methanol extract of Hibiscus rosa sinensis leaves. Int J Pharm Pharm Sci 2013;3:829-30.
108Umana UE, Timbuak JA, Musa SA, Ikyembe DT, Abdurrashid S, Hamman WO. Ulceroprotective effect of methanol extract of Psidium guajava leaves on ethanol induced gastric ulcer in adult Wistar rats. Asian J Med 2012;4:75-8.
109Ahmad H, Wadud A, Jahan N, Khazir M, Sofi G. Evaluation of anti-ulcer activity of hydro alcoholic extract of Post Sumaq (Rhus coriaria Linn.) in Ethanol induced Gastric ulcer in experimental rats. Int J Pharm Pharm Sci 2013;1:7-12.
110Singh S, Majumdar DK. Evaluation of the gastric antiulcer activity of fixed oil of Ocimum sanctum (Holy basil). J Ethnopharmacol 1999;65:13-9.
111Kalra P, Sharma S, Suman, Kumar S. Antiulcer effect of the methanolic extract of Tamarindus indica seeds in different experimental models. J Pharm Bioallied Sci 2011;3:236-41.
112Verma VK, Singh N, Saxena P, Singh R. Anti-ulcer and anti-oxidant activity of Moringa oleifera(Lam) leaves against aspirin and ethanol induced gastric ulcer in rats. Int Res J Pharmaceuticals 2002;2:46-57.
113Kulshreshtha M, Goswami M, Rao CV, Ashwlayan VD, Yadav S. Anti-ulcerogenic potential of Ficus benghalensis leaf, biochemical parameter & histopathological study. J Appl 2011;1:65-8.
114Tamboli FA, More HN. Evaluation of antiulcer and antioxidant activity of Barleria gibsoniDalz. Leaves. Pharmacognosy Res 2016;8:226-30.
115Sahoo SK, Sahoo HB, Priyadarshini D, Soundarya G, Kumar CK, Rani KU, et al. Antiulcer activity of ethanolic extract of Salvadora indica ( W.) leaves on Albino rats. J Clin Diagn Res 2016;10:FF7-10.
116Ahlam HM, Ebtehal MF, Dalia BF. Antiulcer activity of Citharexylum quadrangulare Jacq leaves (ethanolic extract) on experimentally induced gastric ulceration in rats. World J Pharm Pharm Sci 2016;5:145-59.
117Bhajoni PS, Meshram GG, Lahkar M. Evaluation of the antiulcer activity of the leaves of Azadirachta indica: An experimental study. Integr Med Int 2016;3:10-6.
118Bhupesh KV, Alok M, Amita V, Shanti M, Alka V. Preclinical screening of Antiulcer activity of Asparagus racemosus extract on phenylbutazone induced ulceration in experimental animals. J Med Plants Stud 2017;5:348-52.