ArticleWorld journal of gastroenterology2006
Bromophenacyl bromide, a phospholipase A2 inhibitor attenuates chemically induced gastroduodenal ulcers in rats.
Article in World journal of gastroenterology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 11 citations in OpenAlex.
- Serum biomarkers for acute hepatotoxicity of Echis pyramidum snake venom in rats.International journal of clinical and experimental medicine · 2015Article
- Effects of increase in fish oil intake on intestinal eicosanoids and inflammation in a mouse model of colitis.Lipids in health and disease · 2013Article
- Generation in human plasma of misfolded, aggregation-prone electronegative low density lipoprotein.Biophysical journal · 2009Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
aimTo study the effect of bromophenacyl bromide (BPB), a phospholipase A2 inhibitor on gastric secretion and to protect chemically induced gastric and duodenal ulcers in rats.
methodsAcid secretion studies were undertaken in pylorus-ligated rats with BPB treatment (0, 5, 15 and 45 mg/kg). Gastric and duodenal lesions in the rats were induced by ethanol and cysteamine respectively. The levels of gastric wall mucus, nonprotein sulfhydryls (NP-SH) and myeloperoxidase (MPO) were also measured in the glandular stomach of rats following ethanol induced gastric lesions.
resultsBPB produced a dose-dependent inhibition of gastric acid secretion and acidity in rats. Pretreatment with BPB significantly attenuated the formation of ethanol induced gastric lesion. BPB also protected intestinal mucosa against cysteamine-induced duodenal ulcers. The antiulcer activity of BPB was associated with significant inhibition of ethanol-induced depletion of gastric wall mucus, NP-SH and MPO. These findings pointed towards the mediation of sulfhydryls in BPB induced gastrointestinal cytoprotection.
conclusionBPB possesses significant antiulcer and cytoprotective activity against experimentally induced gastroduodenal lesions.
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