{"title":"Gastroprotective Effects of Betahistine Against an Indomethacin-Induced Gastric Mucosal Ulcer in Rats: The Role of CINC-2α Gene.","authors":"Shaghayegh Tarani, Gelareh Vahabzadeh, Hasan Fallah Huseini, Armin Khavandegar, Bahareh Tavakoli-Far, Roshanak Jazayeri","doi":"10.47176/mjiri.38.100","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The role of histamine H3 receptors (H3Rs) in gastric protection and anti-inflammatory function is controversial. In this study, we investigated the gastroprotective effect of a histamine H3 receptor antagonist drug, betahistine, on cytokine-induced neutrophil chemoattractant (CINC) gene expression in a rat model of indomethacin-induced gastric mucosal injury.</p><p><strong>Methods: </strong>In this experiment, rats were divided into four groups; the control group received no treatment, group 2 was treated with indomethacin at a dose of 25 mg/kg, group 3 pre-treated with famotidine at a dose of 50 mg/kg, and group 4 pre-treated with betahistine (as a reference drug) at a dose of 50 mg/kg. The last two groups were followed by indomethacin administration (25 mg/kg), three days later. The obtained values were expressed as the mean and standard error of the mean (mean ± SEM). The level of statistical significance was set at α = 0.05.</p><p><strong>Results: </strong>Indomethacin treatment resulted in large ulcerative lesions with a mean ulcer index of 29± 13.63 mm. However, ulcerative indices were significantly improved in groups pre-treated with famotidine (15.5 ± 8.68 mm; <i>P</i> < 0.05) and betahistine (11±5.66 mm, <i>P</i> < 0.01), compared to the indomethacin-treated group. The expression levels of gastric CINC-2ɑ were significantly elevated in indomethacin-induced groups by 0.028±0.05 in the indomethacin group, 0.005±0.01 in indomethacin + famotidine, and 0.012±0.03 in indomethacin + betahistine groups, compared to the control group (<i>P</i> < 0.05). Besides, pre-treatment with betahistine significantly reduced the expression of CINC-2ɑ induced by indomethacin administration (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>Betahistine for five days before administrating indomethacin reduced the ulcer index and downregulated the expression of CINC-2α significantly. Overall, pre-treatment with betahistine protects against the gastric damage induced by indomethacin by lowering the expression of CINC-2ɑ.</p>","PeriodicalId":18361,"journal":{"name":"Medical Journal of the Islamic Republic of Iran","volume":"38 ","pages":"100"},"PeriodicalIF":0.0000,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11644103/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Journal of the Islamic Republic of Iran","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.47176/mjiri.38.100","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
Background: The role of histamine H3 receptors (H3Rs) in gastric protection and anti-inflammatory function is controversial. In this study, we investigated the gastroprotective effect of a histamine H3 receptor antagonist drug, betahistine, on cytokine-induced neutrophil chemoattractant (CINC) gene expression in a rat model of indomethacin-induced gastric mucosal injury.
Methods: In this experiment, rats were divided into four groups; the control group received no treatment, group 2 was treated with indomethacin at a dose of 25 mg/kg, group 3 pre-treated with famotidine at a dose of 50 mg/kg, and group 4 pre-treated with betahistine (as a reference drug) at a dose of 50 mg/kg. The last two groups were followed by indomethacin administration (25 mg/kg), three days later. The obtained values were expressed as the mean and standard error of the mean (mean ± SEM). The level of statistical significance was set at α = 0.05.
Results: Indomethacin treatment resulted in large ulcerative lesions with a mean ulcer index of 29± 13.63 mm. However, ulcerative indices were significantly improved in groups pre-treated with famotidine (15.5 ± 8.68 mm; P < 0.05) and betahistine (11±5.66 mm, P < 0.01), compared to the indomethacin-treated group. The expression levels of gastric CINC-2ɑ were significantly elevated in indomethacin-induced groups by 0.028±0.05 in the indomethacin group, 0.005±0.01 in indomethacin + famotidine, and 0.012±0.03 in indomethacin + betahistine groups, compared to the control group (P < 0.05). Besides, pre-treatment with betahistine significantly reduced the expression of CINC-2ɑ induced by indomethacin administration (P < 0.05).
Conclusion: Betahistine for five days before administrating indomethacin reduced the ulcer index and downregulated the expression of CINC-2α significantly. Overall, pre-treatment with betahistine protects against the gastric damage induced by indomethacin by lowering the expression of CINC-2ɑ.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
