Stress-related mucosal damage is another common condition that can occur in hospitalized patients leading to PUD. Thus, many post-operative or critically ill patients receive medication to prevent the formation of a stress ulcer, which is also called prophylaxis.

Links to supplementary videos illustrating heartburn and gastric ulcers:. Heartburn [5]. Gastric ulcer [6]. Assessments: Whenever a nurse administers hyperacidity medications, there are common assessments that should be documented, such as an abdominal assessment and documentation of bowel patterns.

During therapy, the nurse should continue to assess for potential medication interactions and side effects and be aware that vitamin B12 malabsorption may occur whenever stomach acidity levels are altered.

Based on the category of medication, renal and liver function may require monitoring. Implementation: The nurse should read the drug label information and follow the recommendations for administering hyperacidity medications with other medications or the intake of food.

Cultural preferences should also be accommodated when safe and feasible because the patient may believe in alternative methods for treating GI discomfort. A written plan of care with modifications for safe use of medications with these alternative methods may be required.

Evaluation: Patients should experience improvement of symptoms within the defined time period; if not, the provider should be notified. There are four major classes of medications used to treat hyperacidity conditions: antacids, H2-receptor antagonists, proton pump inhibitors, and mucosal protectants.

Each class of medication is further described below. Antacids see Figure 7. There are many OTC medications available for this purpose, such as calcium carbonate, aluminum hydroxide, and magnesium hydroxide.

Calcium carbonate is the prototype discussed as an example. Be sure to read drug label information regarding antacids as you administer them because each type has its own specific side effects. Many antacids also contain simethicone, an antiflatulent used for gas relief.

Simethicone is further described in the medication grid below. Antacids neutralize gastric acidity and elevate the pH of the stomach. Elevated pH also inactivates pepsin, a digestive enzyme.

Calcium carbonate comes in various formations such as a tablet, a chewable tablet, a capsule, or liquid to take by mouth. It is usually taken three or four times a day. Chewable tablets should be chewed thoroughly before being swallowed; do not swallow them whole.

The patient should drink a full glass of water after taking either the regular or chewable tablets or capsules. Some liquid forms of calcium carbonate must be shaken well before use. Do not administer calcium carbonate within hours of other medicines because calcium may decrease the effectiveness of the other medicine.

Calcium carbonate may be contraindicated in patients with preexisting kidney disease because it may cause hypercalcemia. Common side effects of calcium carbonate include constipation and rebound hyperacidity when it is discontinued. Other interventions to prevent hyperacidity can also be recommended, such as smoking cessation and avoiding food and beverages that can cause increased acidity alcohol, high-fat or spicy foods, and caffeine.

A common H2-receptor antagonist is famotidine. It is available OTC and is also often prescribed orally or as an IV injection in the hospital setting.

Other H2-receptor antagonists include cimetidine and ranitidine. Cimetidine has a high risk of drug interactions, especially in elderly patients because of its binding to cytochrome P enzymes in the liver, which affects the metabolism of other drugs.

Famotidine see Figure 7. OTC famotidine is also used to treat heartburn or sour stomach. To prevent symptoms, oral famotidine is taken 15 to 60 minutes before eating foods or drinking drinks that may cause heartburn.

Preexisting liver and kidney disease may require dosage adjustment. Famotidine is supported by evidence as safe for use in pediatric patients younger than 1 year old, as well as in geriatric patients.

Patients taking the oral suspension should be instructed to shake it vigorously for 5 to 10 seconds prior to each use. Additionally, smoking interferes with histamine antagonists and should be discouraged. A common proton pump inhibitor PPI is pantoprazole see Figure 7. It may be prescribed in various routes including orally, with an NG tube, or as an IV injection in the hospital setting.

Other PPIs include esomeprazole, lansoprazole, and omeprazole. PPIs are more powerful than antacids and H2-receptor antagonists.

Pantoprazole is used to treat damage from gastroesophageal reflux disease GERD in adults and children five years of age and older by allowing the esophagus to heal and prevent further damage. It is also used to treat conditions where the stomach produces too much acid, such as Zollinger-Ellison syndrome in adults.

PPIs may also be given in combination with antibiotics to treat H. Pylori infections, a common cause of duodenal ulcers. pylori leading successful induction of ulcers up to 9th week in all groups.

pylori were observed up to 5th, 6th and 3rd week, respectively. However, C. group exhibited mild inflammation, congestion and presence of H. pylori were observed up to 3rd, 5th and 9th week, respectively, which was reduced to 3rd, 5th and 4th week, respectively, in the highest dose to C.

as shown in Fig. In the present investigation, the various groups of animals were treated prophylactically with the C. zeylanica extract to determine its ulcer protective potential. Naproxen was used as the ulcerogenic tool to produce acute gastric lesions, and it is due to non-selective inhibition of cyclooxygenase I and II, leading to reduced PGE2 synthesis and decreased mucus secretion [ 39 ].

Results showed that C. Our results are in accordance with the observations of Halter et al. Its ulcerogenic potential was exhibited due to the hyper secretion of histamine from the parietal cells of the gastric mucosa, particularly in the glandular portion. A large area of redness devoid of any perforations was observed in the glandular potion of stomach which is characteristic of histamine-induced ulcers [ 41 ].

It is evident that the C. zeylanica extract may act by blocking H 2 receptors. Our findings are in accordance with those of Warzecha et al. Our results were in agreement with the study of Narra et al. evaluated antiulcer activity of Cucumis Sativus fruit extract. It was significantly reduced ulcer index in animals [ 42 ].

Ethanol produces acute experimental gastric lesions due to generation of free radicals primarily superoxide anions, hydroxyl radicals, lipid peroxidases localized inflammatory changes [ 43 ]. dose of ethanol as the ulcerogenic tool [ 34 ].

The various groups of animals were treated prophylactically with the drugs to determine the ulcer healing potential of the C. However, results showed that the C. zeylanica extract was unable to protect the gastric mucosal damage at all the three doses.

Capparis zeylanica extract was very weak in amelioration of ethanol-induced gastric lesions when compared with sucralfate, which confirmed that the drug does not have any cement-like or ulcer painting activity [ 44 ].

The results of Srivasta et al. indicated that fruit extract of Cucumis melo Var. Momordica Roxb. was useful in the ethanol-induced ulcer model in rats. It was significantly reduced acid secretion and thus reduced ulcer index [ 45 ].

Table 8 shows the comparative study of antiulcer activity of our finding with previous publications [ 46 , 47 , 48 ]. In the present investigation, naproxen-induced and H.

pylori -infected ulcer model was used to evaluate the ulcer healing and antimicrobial potential of the C. zeylanica extract [ 35 ]. When H. pylori is administered by oral gavage, this panmictic, spiral, gram negative organism resides in the disrupted mucosa for a long time exhibiting its ulcerogenic and oncopathogenic effects.

Hence, this model is best suited to evaluate the antiulcer and anti- H. pylori effect of any drug [ 49 ]. The oncopathogenic effects of H. pylori are due to overexpression of COX2 mRNA leading to altered cellular kinetics programmed cell death tumor angiogenesis and increased in the amount of nitrotyrosine leading to a precancerous which later culminates to produce metaplastic lesions [ 50 ].

The infection status was determined using rapid urease test and molecular confirmation by DNA extraction and amplification of 16sr RNA and hrg Agene [ 36 ]. The animals treated with C. showed rapid healing and amelioration of infection within 4 weeks of treatment.

This signifies the weak antimicrobial activity of C. over a period of 9 weeks. The present study suggests that the C. zeylanica extract possesses potent antiulcer activity against chemicals-induced ulcer with significant antimicrobial activity. The extract showed effectivity in both acute and chronic ulcers by reducing area of ulcers.

Capparis zeylanica extract significantly restored the morphology of ulcerated stomach to normal one. Thus, ethanolic extract of C. zeylanica leaves may be considered as a potential therapeutic candidate in gastric ulcers infected with H.

It can be developed into suitable formulation after clinical trials. Jain P Secondary metabolites for antiulcer activity. Nat Prod Res 30 6 — Article CAS PubMed Google Scholar. Inform Med Unlocked —4.

Article Google Scholar. Najm WI Peptic ulcer disease. Prim Care Clin Off Pract 38 3 — Napolitano L Refractory peptic ulcer disease. Gastroenterol Clin N Am 38 2 — Kempenich JW Acid peptic disease.

Surg Clin N Am 98 5 — Article PubMed Google Scholar. Lim W, Subramaniam M, Abdin E, Vaingankar J, Ann S Peptic ulcer disease and mental illnesses. Gen Hosp Psychiatry 36 1 — Urs AN, Thomson M Peptic ulcer disease. Paediatr Child Health Oxf 24 11 — Awaad AS, El-meligy RM, Soliman GA Natural products in treatment of ulcerative colitis and peptic ulcer.

J Saudi Chem Soc 17 1 — Article CAS Google Scholar. Jain P, Satapathy T, Pandey RK Rhipicephalus microplus acari: Ixodidae : Clinical safety and potential control by topical application of cottonseed oil Gossypium sp. on cattle. Exp Parasitol Jain P, Satapathy T, Pandey RK Efficacy of arecoline hydrobromide against cattle tick Rhipicephalus Boophilus microplus.

Int J Acarol 46 4 — Jain P, Satapathy T, Pandey RK First report on ticks Acari: Ixodidae controlling activity of cottonseed oil Gossypium Sp. Jain P, Satapathy T, Pandey RK Rhipicephalus microplus : a parasite threatening cattle health and consequences of herbal acaricides for upliftment of livelihood of cattle rearing communities in Chhattisgarh.

Biocatal Agric Biotechnol Rao SP, Jain P, Rathore P, Singh VK Larvicidal and knockdown activity of Citrus limetta Risso oil against dengue virus vector. Indian J Nat Prod Resour 7 3 — Google Scholar.

Kumar V, Jain P, Rathore K, Ahmed Z Biological evaluation of Pupalia lappacea for antidiabetic, antiadipogenic, and hypolipidemic activity both in vitro and in vivo. Article PubMed PubMed Central Google Scholar. Pandey RK, Shukla SS, Vyas A, Jain V, Jain P, Saraf S Fingerprinting analysis and quality control methods of herbal medicines.

CRC Press, Boca Raton. Book Google Scholar. Jain P, Pandey R, Shukla SS Inflammation: Natural resources and its applications. Springer briefs. Springer, New Delhi. Kumar V, Rathore K, Jain P, Ahmed Z Biological activity of bauhinia racemose against diabetes and interlinked disorders like obesity and hyperlipidemia.

Clin Phytosci Singh P, Jain P, Pandey R, Shukla SS Phytotherapeutic review on diabetes. Spatula DD. Sharwan G, Jain P, Pandey R, Shukla SS Toxicity and safety profiles of methanolic extract of Pistacia integerrima J.

Stewart ex Brandis PI for Wistar Rats. J Pharmacopunct 19 3 — Jain P, Rao SP, Singh V, Pandey R, Shukla SS Acute and sub-acute toxicity studies of an ancient ayurvedic formulation: agnimukha churna.

Columbia J Pharm Sci — Jain P, Pandey R, Shukla SS Reproductive and developmental toxicity study of talisadya churna: an ancient polyherbal formulation.

IAJPR 6 5 — CAS Google Scholar. Jain P, Pandey R, Shukla SS Acute and subacute toxicity studies of polyherbal formulation talisadya churna in experimental animal model. MJPMS 1 1 :7— Sharwan G, Jain P, Pandey R, Shukla SS Toxicity profile of traditional herbal medicine.

J Ayu Herb Med 1 3 — Zinatloo-Ajabshir Z, Zinatloo-Ajabshir S Preparation and characterization of curcumin niosomal nanoparticles via a simple and eco-friendly route. J Nanostruct 9 4 — Ghule BV, Murugananthan G, Yeole PG Analgesic and antipyretic effects of Capparis zeylanica leaves.

Fitoterapia 78 5 — Arulmozhi P, Vijayakumar S, Kumar T Microbial pathogenesis phytochemical analysis and antimicrobial activity of some medicinal plants against selected pathogenic microorganisms. Microb Pthogenes — Arulmozhi P, Vijayakumar S, Praseetha PK, Jayanthi S Extraction methods and computational approaches for evaluation of antimicrobial compounds from Capparis zeylanica L.

Anal Biochem — Tlili N, Elfalleh W, Saadaoui E, Khaldi A, Triki S, Nasri N The caper Capparis L. Fitoterapia 82 2 — Haque ME, Haque M, Rahman MM, Rahman MM, Khondkar P, Wahed M, Mossadik MA, Gray AI, Sarker SD E-octadecenynoic acid from the roots of Capparis zeylanica.

Fitoterapia 75 2 — Article PubMed CAS Google Scholar. Sini KR, Sinha BN, Rajasekaran A Protective effects of Capparis zeylanica Linn. leaf extract on gastric lesions in experimental animals.

Avicenna J Med Biotechnol 3 1 — PubMed PubMed Central Google Scholar. OECD OECD guideline for testing of chemicals: acute oral toxicity—acute toxic class method. OECD Guidel Test Chem — Satoh H, Guth PH, Grossman MI Roll of food in gastrointestinal ulceration produced by food in the rat.

Gastroenterol — Sirmagul B, Kilic FS, Batu O, Erol K The effects of verapamil on stress and histamine induced gastric lesions in rats. Meth Exp Clin Pharmacol Sheeba MS, Asha VV Effect of Cardiospermum halicacabum on ethanol-induced gastric ulcers in rats.

J Ethnopharmacol — Kalies I, Li H, Mellgard B A rat model of chronic H. pylori infection. Studies of epithelial cell turn over and gastric ulcer healing. Scand J Gastroenterol — Ibrahim M, Khan AA, Tiwari SK, Khaja MN, Habeeb AK, Habibullah CM Antimicrobial activity of Sapindus mukorossi and Rheum emodi extracts against H.

pylori : in vitro and in vivo studies. World J Gastroenterol 12 44 — Article CAS PubMed PubMed Central Google Scholar. Tiwari SK, Khan AA, Manoj G, Ahmed S, Abid Z, Habeeb A et al A simple multiplex PCR assay for diagnosing virulent Helicobacter pylori infection in human gastric biopsy specimens from subjects with gastric carcinoma and other gastro-duodenal diseases.

J Appl Microbiol 6 — Kaur M, Singh A, Kumar B Comparative antidiarrheal and antiulcer effect of the aqueous and ethanolic stem bark extracts of Tinospora cordifolia in rats.

J Adv Pharm Technol Res 5 3 — Lichtenberger LM, Wang ZM, Romero JJ, Ulloa C, Perez JC, Giraud MN Non-steroidal anti-inflammatory drugs NSAIDs associate with zwitterionic phospholipids: insight into the mechanism and reversal of NSAID-induced gastrointestinal injury.

Nat Med — Halter F, Tarnawski AS, Schmassmann A, Peskar BM Cyclooxygenase 2-implications on maintenance of gastric mucosal integrity and ulcer healing: controversial issues and perspectives.

Gut 49 3 — Warzecha Z, Dembinski A, Brozozowski-Ceranowicz P, Konturek SJ Histamine in stress ulcer prophylaxis in rats. J Physiol Pharmacol 52 3 — CAS PubMed Google Scholar.

Narra S, Nisha KS, Nagesh HS Evaluation of antiulcer activity of hydroalcoholic fruit pulp extract of Cucumis sativus. Int J Pharm Sci Res 6 11 — Bhattacharyya A, Chattopadhyay R, Mitra S, Crowe SE Oxidative stress: an essential factor in the pathogenesis of gastrointestinal mucosal diseases.

Physiol Rev 94 2 — Uchida M, Keiko K Yogurt containing Lactobacillus gasseri OLL exerts gastroprotective action agaisnt acute gastric lesion and antral ulcers in rats.

J Pharmacol Sci — Srivastava A, Mukerjee A, Ramteke P, Pandey H, Mishra DS Antiulcer potential of Cucumis melo Var.

J Pharm Res — Sharma A Antiulcer activity of methanolic extract of leaf of tylophora indica on histamine and naproxen induced gastric lesions in rats.

Pharmacologyonline — Achukwu DC, Eze AA Anti-ulcer activity of the leaf extracts of borreria ocymoides in rats. Biol Res 7 6 — Abebaw M, Mishra B, Gelayee DA Evaluation of anti-ulcer activity of the leaf extract of Osyris quadripartita Decne.

Santalaceae in rats. J Exp Pharmacol — Yoshida N, Sugimoto N, Hirayama F, Nakamura Y, Ichikawa H, Naito Y, Yoshikawa T Helicobacter pylori infection potentiates aspirin induced gastric mucosal injury in Mongolian gerbils. Gut — Tsuji S, Tsuji M, Murata H, Nishida T, Kamori M, Yasumara M, Ishli S, Sasayama Y, Kawanio S, Hayashi M Helicobacter pylori eradication to prevent gasric cancer; underlying molecular and cellular mechanisms.

World J Gasteroenterol 12 11 — Download references. The authors are thankful to the institute providing laboratory facilities. We are extending our gratitude toward Probecell: Scientific Writing Services for proofreading and editing of the manuscript.

Department of Pharmaceutical Sciences, United Institute of Pharmacy, Naini, Allahabad, , India. You can also search for this author in PubMed Google Scholar. All authors have read and approved the manuscript. Apart from that, many adverse effects have been addressed in relation to continuous use of the drugs such as arrhythmia, hypomagnesemia, hypersensitivity, impotence and gynecomastia [ 9 ].

In addition, some of these medications are costly [ 10 ] and have high risk of causing gastric cancer and later stage disease [ 11 ]. Thus, this enigma has encouraged the researchers to identify a new therapeutically safe and effective treatment to completely eradicate the issue.

From this perspective, plants are gaining importance as they are the major contributors of bioactive molecules having anti-ulcerogenic properties [ 12 ]. Among medicinal plants, oils derived from plant species are also gaining wide popularity for their therapeutic properties.

Recently, several studies have reported on the effectiveness of virgin coconut oil VCO in treating and preventing peptic ulcer disease significantly as compared to commercial coconut oil, also known as copra oil CO [ 13 ]. The major differences between VCO and CO are due to the extraction method, which leads to differences in their benefits.

Virgin coconut oil is classified as oil extracted from fresh-dry mature kernel of coconut Cocos nucifera L. As the production process does not involve heat, VCO does not go through any transformation and thus retains the beneficial components such as vitamins, antioxidants, the fatty acid component lauric acid and other medium chain fatty acids MCFA which help in digestion [ 15 ].

Moreover, VCO is an edible food which can be included in our diet and taken directly without prescription from a physician, without causing any side effects.

Although studies have reported on the effects of VCO on peptic ulcer [ 13 ], there has been no study yet to elucidate the mechanism involved in inhibiting ulceration. The present study aims to reveal the possible mechanism involved in the action of VCO in ulcerative models. Low temperature technique was applied in the preparation of VCO.

The solid endosperm of matured fresh coconut was crushed and made into a viscous slurry [ 16 ]. It was later mechanically squeezed through a cheese cloth to collect the coconut milk.

The milk was kept in the refrigerator and frozen for 48 h, then heated at °C using a thermostat oven. After the heating process, the collected oil was filtered using a cheese cloth.

All chemicals and solvents were of analytical grade and included omeprazole Sigma Aldrich, St. Louis, MD, USA , ethanol Merck, UK , phenolphthalein Merck, UK , alcian blue Merck, UK , magnesium chloride Merck, UK , sucrose Merck, UK and sodium citrate Merck, UK.

A total of 72 Wistar rats 40 days old , weighing — g, were obtained from our animal feeding center. All studies carried out were approved by the animal care and ethical committee following the employed protocols ACUC No: HDFY-LL The animals were kept at room temperature 25—28°C for a minimum of seven days for acclimatization to room conditions prior to the experimental procedure.

The experimental rats were divided into three groups consisting of 6 rats per group. The grouping was the same for each ulcer induction model. On day 8, the rats were paralyzed by strapping the fore and hind limbs on a flat wooden plank, and transferred into the refrigerator 4—6°C.

After two hours, the rats were sacrificed by cervical dislocation. The stomach was incised along the greater curvature and the lumen was rinsed with normal saline. The ulcer scoring was carried out based on the method described by Minano et al. The acquired supernatant was used to study activity using an antioxidant enzyme assay.

The experimental rats of each group were pre-treated as explained previously for 7 days and fasted for 24 h into the eighth day. After 1 h of ulcer induction, the animals were sacrificed by cervical dislocation. The stomach was dissected out for the macroscopic examination of ulcers.

The scoring for ulcer was determined using a method described in a previous study. Another set of rats were pre-treated for 7 days as described earlier. The animals were then fasted for 24 h into the eighth day. After 6 h of piroxicam induction, the animals were sacrificed by cervical dislocation.

The rats were dissected and their stomachs were cut open along the greater curvature. The gastric lumen was rinsed with normal saline and examined.

The ulcer scoring was carried out using a method described in a previous study. Animals were pre-treated for a period of seven days as described earlier and the rats were fasted for 24 h into the eighth day to ensure complete emptying of the stomach and water was permitted ad libitum.

After anesthetic, the abdomen was opened and pylorus ligation was carried out without causing any damage to its blood supply. Then, the stomach was replaced carefully and the abdominal wall was closed in two layers with interrupted sutures followed with a moist swab of normal saline.

After 4 h, each stomach was dissected out and cut open along the greater curvature [ 26 , 27 ]. The ulcer index UI was determined using the scoring scaling of Minano et al. After dissection and removal of the stomach, gastric juice was collected. Than it was centrifuged for 5 min at × g, while the supernatant was separated and used to analyze for pH, gastric juice volume, and total acidity.

Total acid was estimated by titrating against 0. Gastric mucus content was determined using the method described by Corne et al. The stomach was removed, opened along the lesser curvature, and rinsed with cold saline. The levels of superoxide dismutase SOD , glutathione reductase GR , glutathione peroxidase GP , catalase CAT , malondialdehyde MDA and nitrite were determined using a commercially available ELISA kit Cayman, USA [ 30 ].

All the grouped data were presented as mean ± standard error of the mean SEM. The percentage of inhibition was Anti-ulcer effects of virgin coconut oil VCO on cold-stress-induced rats.

Comparatively, the percentage of inhibition for the omeprazole-treated group was As reported above, similar trends were observed for the piroxicam-induced ulcer model. The highest UI 3. Anti-ulcer effects of virgin coconut oil VCO on piroxicam-induced rats. In the pylorus experimental model, VCO evoked gastric acid secretion in rats.

The gastric juice induced by VCO showed significant reduction of total acidity and ulcer scoring. On the other hand, the total acid, for the negative control reported as The gastric mucus content of pylorus ligation negative control rats was 4.

The pH for the negative control group was found to be 2. The UI for the negative control group was 4. The percentage of inhibition noted for the positive control group versus the pylorus-ligated group was Anti-ulcer effects of virgin coconut oil VCO on pylorus ligated model.

negative control. The level of PGE 2 content in the negative control was Anti-ulcer effect of virgin coconut oil VCO on prostaglandin E 2 PGE 2 synthesis.

Different factors are involved in the pathogenesis of peptic ulcer in human beings such as chronic use of NSAIDs, stress, H. pylori infection, alcohol consumption, smoking and inappropriate dietary lifestyle. Although various kinds of medication are available to treat peptic ulcer disease such as H-2 receptor antagonist, proton pump inhibitors PPIs , antacids and anti-muscarinics [ 32 ], most of them cause side effects to patients, yet do not providing a complete recovery [ 33 ].

Earlier studies revealed the effectiveness of VCO in treating ulcer in animal models [ 13 , 19 ]. In the last decade, the exploitation of VCO for their fatty acid and vitamin E composition followed by antioxidant properties and their effects on various ailments have been reported by researchers [ 15 , 16 ].

There has been growing interest and attention on VCO and their potential effects on humans include anti-microbial, anti-viral, anti-diabetic, hypocholesterolemic [ 16 ] and anti-ulcer effect.

To the best of our knowledge, no detailed study has been conducted on different ulcer models that elucidated the possible mechanism. Therefore, the present study was designed to further evaluate the antiulcer activity of VCO compared to a standard drug omeprazole.

For this purpose, the effects of VCO were evaluated using different ulcer models induced by cold restraint stress, ethanol, piroxicam NSAIDs , ethanol and pylorus ligation. Moreover, the effects of VCO on the gastric secretions from a pylorus-ligated model, level of PGE 2 secretion from a piroxicam model and antioxidant assays from an ethanol-induced model were also studied.

Omeprazole is an extensively used anti-ulcer drug belonging to proton pump inhibitors PPIs , to treat peptic ulcer disease caused by stress, non-steroidal anti-inflammatory drugs and by H. pylori infections [ 34 ]. However, another study revealed that omeprazole acts as a potent antioxidant to scavenge the oxygen free radical and prevents oxidative damage by increasing lipid peroxidation and protein oxidation, in an experiment conducted using three different ulcer models, stress, indomethacin-induced and pylorus ligation-induced models [ 35 ].

Thus, in the present investigation omeprazole was chosen as the standard drug for the positive control treated group. Stress-induced ulcer may be caused by histamine secretion by the parietal cells. In addition, presence of reactive oxygen species ROS due to stress also may provoke damage to he stomach leading to ulceration.

Apart from that, acid and pepsin-associated factors also play a role in the pathogenesis of stress-induced ulcer. Increase in generation of ROS during stress will lead to oxidative damage and cause injury to the mucosal layer. Stress-induced ulcer also leads to a decrease in mucus production.

Stress-related mucosal damage is another common condition that can occur in hospitalized patients leading to PUD. Thus, many post-operative or critically ill patients receive medication to prevent the formation of a stress ulcer, which is also called prophylaxis. Links to supplementary videos illustrating heartburn and gastric ulcers:.

Heartburn [5]. Gastric ulcer [6]. Assessments: Whenever a nurse administers hyperacidity medications, there are common assessments that should be documented, such as an abdominal assessment and documentation of bowel patterns.

During therapy, the nurse should continue to assess for potential medication interactions and side effects and be aware that vitamin B12 malabsorption may occur whenever stomach acidity levels are altered. Based on the category of medication, renal and liver function may require monitoring.

Implementation: The nurse should read the drug label information and follow the recommendations for administering hyperacidity medications with other medications or the intake of food. Cultural preferences should also be accommodated when safe and feasible because the patient may believe in alternative methods for treating GI discomfort.

A written plan of care with modifications for safe use of medications with these alternative methods may be required. Evaluation: Patients should experience improvement of symptoms within the defined time period; if not, the provider should be notified.

There are four major classes of medications used to treat hyperacidity conditions: antacids, H2-receptor antagonists, proton pump inhibitors, and mucosal protectants. Each class of medication is further described below. Antacids see Figure 7. There are many OTC medications available for this purpose, such as calcium carbonate, aluminum hydroxide, and magnesium hydroxide.

Calcium carbonate is the prototype discussed as an example. Be sure to read drug label information regarding antacids as you administer them because each type has its own specific side effects.

Many antacids also contain simethicone, an antiflatulent used for gas relief. Simethicone is further described in the medication grid below. Antacids neutralize gastric acidity and elevate the pH of the stomach. Elevated pH also inactivates pepsin, a digestive enzyme.

Calcium carbonate comes in various formations such as a tablet, a chewable tablet, a capsule, or liquid to take by mouth.

It is usually taken three or four times a day. Chewable tablets should be chewed thoroughly before being swallowed; do not swallow them whole. The patient should drink a full glass of water after taking either the regular or chewable tablets or capsules.

Some liquid forms of calcium carbonate must be shaken well before use. Do not administer calcium carbonate within hours of other medicines because calcium may decrease the effectiveness of the other medicine.

Calcium carbonate may be contraindicated in patients with preexisting kidney disease because it may cause hypercalcemia. Common side effects of calcium carbonate include constipation and rebound hyperacidity when it is discontinued.

Other interventions to prevent hyperacidity can also be recommended, such as smoking cessation and avoiding food and beverages that can cause increased acidity alcohol, high-fat or spicy foods, and caffeine.

A common H2-receptor antagonist is famotidine. It is available OTC and is also often prescribed orally or as an IV injection in the hospital setting. Other H2-receptor antagonists include cimetidine and ranitidine.

Cimetidine has a high risk of drug interactions, especially in elderly patients because of its binding to cytochrome P enzymes in the liver, which affects the metabolism of other drugs. Famotidine see Figure 7.

OTC famotidine is also used to treat heartburn or sour stomach. To prevent symptoms, oral famotidine is taken 15 to 60 minutes before eating foods or drinking drinks that may cause heartburn. Preexisting liver and kidney disease may require dosage adjustment.

Famotidine is supported by evidence as safe for use in pediatric patients younger than 1 year old, as well as in geriatric patients. Patients taking the oral suspension should be instructed to shake it vigorously for 5 to 10 seconds prior to each use. Additionally, smoking interferes with histamine antagonists and should be discouraged.

A common proton pump inhibitor PPI is pantoprazole see Figure 7. It may be prescribed in various routes including orally, with an NG tube, or as an IV injection in the hospital setting.

Other PPIs include esomeprazole, lansoprazole, and omeprazole. PPIs are more powerful than antacids and H2-receptor antagonists. Pantoprazole is used to treat damage from gastroesophageal reflux disease GERD in adults and children five years of age and older by allowing the esophagus to heal and prevent further damage.

It is also used to treat conditions where the stomach produces too much acid, such as Zollinger-Ellison syndrome in adults. PPIs may also be given in combination with antibiotics to treat H.

Pylori infections, a common cause of duodenal ulcers. Antiulcer medications: Mechanism of action, pharmacology, and side effects. Formulary drug information for this topic.

No drug references linked in this topic. Find in topic Formulary Print Share. View in. Language Chinese English. Author: Nimish B Vakil, MD, AGAF, FACP, FACG, FASGE Section Editor: Mark Feldman, MD, MACP, AGAF, FACG Deputy Editor: Shilpa Grover, MD, MPH, AGAF Literature review current through: Jan This topic last updated: Apr 19, pylori , withdrawal of nonsteroidal anti-inflammatory drugs NSAIDs , and antisecretory drugs are the mainstays of treatment for peptic ulcer disease.

To continue reading this article, you must sign in with your personal, hospital, or group practice subscription. Subscribe Sign in. It does NOT include all information about conditions, treatments, medications, side effects, or risks that may apply to a specific patient.

It is not intended to be medical advice or a substitute for the medical advice, diagnosis, or treatment of a health care provider based on the health care provider's examination and assessment of a patient's specific and unique circumstances.

Al Batran, R. In vivo antioxidant and antiulcer activity of Parkia speciosa ethanolic leaf extract against ethanol-induced gastric ulcer in rats. PLoS One 8 5 , CrossRef Full Text Google Scholar. Almasaudi, S. Antioxidant, anti-inflammatory, and antiulcer potential of Manuka Honey against gastric ulcer in rats.

Ansari, S. In vivo , proteomic, and in- silico investigation of Sapodilla for therapeutic potential in gastrointestinal disorders. Arab, H. Diosmin protects against ethanol-induced gastric injury in rats: Novel anti-ulcer actions. PLoS One 10 3 , Augusto, A.

Oxidative stress expression status associated to Helicobacter pylori virulence in gastric diseases. Foroumadi, A. Synthesis and anti- Helicobacter pylori activity of 5- nitroaryl -1, 3, 4-thiadiazoles with certain sulfur containing alkyl side chain. Franke, A. Alcohol-related diseases of the esophagus and stomach.

Fu, Y. Gim, S. Curcumin attenuates the middle cerebral artery occlusion-induced reduction in γ-enolase expression in an animal model. Graham, D. History of Helicobacter pylori , duodenal ulcer, gastric ulcer and gastric cancer.

World J. He, H. Irshad, N. Antihyperlipidemic effect of selected pyrimidine derivatives mediated through multiple pathways. Jakhar, R. Relevance of molecular docking studies in drug designing. Li, W. Protective effect of chelerythrine against ethanol-induced gastric ulcer in mice.

Liu, B. Liu, Y. Protective effect of l-citrulline against ethanol-induced gastric ulcer in rats. Lu, L. Brucine: A review of phytochemistry, pharmacology and toxicology. Luo, X. Expression of apoptosis-associated microRNAs in ethanol-induced acute gastric mucosal injury via JNK pathway.

Alcohol 47 6 , — Mahmoud, Y. Spirulina ameliorates aspirin-induced gastric ulcer in albino mice by alleviating oxidative stress and inflammation. McGarry, T. Hypoxia, oxidative stress and inflammation. Free Radic. Nayarisseri, A. Experimental and computational approaches to improve binding affinity in chemical biology and drug discovery.

Park, S. Artemisia asiatica extracts protect against ethanol-induced injury in gastric mucosa of rats. Poonam, D. Cyclo-oxygenase-2 expression and prostaglandin E2 production in experimental chronic gastric ulcer healing. Qazi, N. Anti-diarrheal, anti-secretory, anti-spasmodic and anti-ulcer activities of Acacia Modesta Mimosaceae aerial parts.

Qin, J. Anti-tumor effects of brucine immuno-nanoparticles on hepatocellular carcinoma. Nanomedicine 7 1 , — Richardson, P. Proton pump inhibitors. Pharmacology and rationale for use in gastrointestinal disorders..

Drugs 56 1 , — Salga, M. Gastroprotective activity and mechanism of novel dichlorido-zinc II 2- 5-methoxybenzylideneamino ethyl piperaziniumphenolat e complex on ethanol-induced gastric ulceration.

Saraswati, S. Anticarcinogenic effect of brucine in diethylnitrosamine initiated and phenobarbital-promoted hepatocarcinogenesis in rats. Seifi, B. Evaluation of renal oxidative stress in the development of DOCA-salt induced hypertension and its renal damage.

Tabiri, S. Assessment of the environmental risk factors for a gastric ulcer in northern Ghana.. Pan Afr. Tandon, R. Oxidative stress and antioxidants status in peptic ulcer and gastric carcinoma. Indian J.

PubMed Abstract Google Scholar. Tulassay, Z. Effect of esomeprazole triple therapy on eradication rates of Helicobacter pylori , gastric ulcer healing and prevention of relapse in gastric ulcer patients.

Wang, Y. Multipathway integrated adjustment mechanism of Glycyrrhiza triterpenes curing gastric ulcer in Rats. Yeo, D. The aqueous extract from Artemisia capillaris inhibits acute gastric mucosal injury by inhibition of ROS and NF-kB.

Yin, W. Analgesic and anti-inflammatory properties of brucine and brucine N-oxide extracted from seeds of Strychnos nux-vomica.. Zamani, M.

Zhang, L. Effects of cigarette smoke and its active components on ulcer formation and healing in the gastrointestinal mucosa. Zhang, Q. Pat, and its effects on gastric cancer cells. Fitoterapia 89 1 , — Zhang, S. Phytomedicine 21 11 , — Zhou, F. Liraglutide attenuates lipopolysaccharide-induced acute lung injury in mice.

Keywords: brucine, anti-ulcer, anti- H. Citation: Noman M, Qazi NG, Rehman NU and Khan A-u Pharmacological investigation of brucine anti-ulcer potential. doi: Received: 28 February ; Accepted: 13 July ; Published: 17 August Copyright © Noman, Qazi, Rehman and Khan.

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