The Effect of Metformin on Ethanol- and IndomethacinInduced Gastric Ulcers in Rats.

Betül Esra İpek, Meral Yüksel, Alev Cumbul, Feriha Ercan, Hülya Cabadak, Banu Aydın, İnci Alican
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引用次数: 5

Abstract

Background: Previous studies found metformin as an effective agent to suppress oxidative stress, inflammation, and apoptosis in various inflammatory diseases. The present study investigated the effect of metformin against 2 experimental gastric injury models in rats, using macroscopical, histopathological, biochemical, and immunostaining studies.

Methods: After 24 hours of fasting, male Sprague-Dawley rats (280-400 g) (n = 8 per group) received indomethacin (80 mg/kg; indo ulcer group) or absolute ethanol (5 mL/kg; ethanol ulcer group) or vehicle orally by gavage. Metformin (500 mg/kg) was given orally for 3 days prior to indomethacin or ethanol challenge. Ranitidine (50 mg/kg) was given orally for 3 days before indomethacin or ethanol administration as a positive control. On day 3, the animals were euthanized 6 hours after indo or 1 hour after ethanol challenge. Gastric samples were used for macroscopic scoring, histopathological examinations, and biochemical assays. Trunk blood was collected for the assessment of interleukin-1β level.

Results: In both ethanol ulcer and indo ulcer groups, metformin decreased the extent of gastric lesions macroscopically and microscopically, improved the high chemiluminescence levels, and the percentage of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive apoptotic cells compared with untreated ulcer groups. Gastric blood flow analysis revealed significant increases in both metformin-treated ulcer groups compared to untreated ulcer groups.

Conclusion: The findings of the present work demonstrated the gastroprotective effect of metformin against the development of gastric mucosal lesions induced by ethanol and indomethacin in non-diabetic, normoglycemic rats via its antioxidant and anti-apoptotic properties and partly from its ability to restore blood flow.

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二甲双胍对乙醇和吲哚美辛诱导大鼠胃溃疡的影响。
背景:已有研究发现二甲双胍可有效抑制各种炎症性疾病的氧化应激、炎症和细胞凋亡。本研究采用宏观、组织病理学、生化和免疫染色等方法研究二甲双胍对2种大鼠实验性胃损伤模型的影响。方法:禁食24 h后,雄性sd大鼠(280 ~ 400 g)(每组8只)给予吲哚美辛(80 mg/kg;溃疡组)或无水乙醇(5ml /kg;乙醇溃疡组)或整车灌胃。二甲双胍(500 mg/kg)口服3天,然后给药吲哚美辛或乙醇。雷尼替丁(50 mg/kg)口服3天,然后给药吲哚美辛或乙醇作为阳性对照。在第3天,动物在注射后6小时或乙醇注射后1小时被安乐死。胃标本用于宏观评分、组织病理学检查和生化分析。采集干血检测白细胞介素-1β水平。结果:在乙醇性溃疡和印陀溃疡组,与未治疗的溃疡组相比,二甲双胍降低了胃损伤的宏观和微观范围,提高了高化学发光水平和末端脱氧核苷酸转移酶dUTP缺口末端标记(TUNEL)阳性的凋亡细胞百分比。胃血流分析显示,与未治疗的溃疡组相比,二甲双胍治疗组的胃血流明显增加。结论:二甲双胍对非糖尿病、血糖正常的大鼠胃粘膜病变具有抗氧化和抗凋亡的保护作用,部分原因是其恢复血流的能力。
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