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甲巯咪唑可预防大鼠应激和化学诱导的胃病。

Methimazole prevents stress and chemical induced gastropathy in rats.

作者信息

Al Moutaery Ahmed

机构信息

Clinical Biochemistry Division, Department of Pathology, Armed Forces Hospital, Riyadh, Kingdom of Saudi Arabia.

出版信息

Exp Toxicol Pathol. 2003 Nov;55(4):277-85. doi: 10.1078/0940-2993-00325.

Abstract

This investigation was undertaken to study the effect of methimazole (MMI) on gastric acid secretion and stress and chemically induced gastric ulcer in rats. Acid secretion studies were undertaken using pylorus-ligated rats pretreated with MMI (10-100 mg/kg, i.p.). The effect of orally administered MMI on water-immersion restraint (WIR) stress, indomethacin and ethanol-induced gastric ulcers was also tested. The level of myeloperoxidase (MPO), non-protein sulfhydryls (NP-SH) and gastric wall mucus was measured in the glandular stomach of rats following ethanol-induced gastric lesions. There was a dose-dependent inhibition of gastric acid secretion and ulcerogen induced gastric lesion formation in the MMI treated rats. Our morphological and histological studies showed a complete prevention of ethanol-induced lesions in the rats treated with high dose (100 mg/kg) of MMI. A significant attenuation of ethanol-induced increase in gastric MPO activity, depletion of NP-SH and reduction of gastric wall mucus was also observed in MMI treated rats. These findings clearly suggest the involvement of endogenous pro-inflammatory agents and oxidative stress in mediating the gastroprotective effect of MMI.

摘要

本研究旨在探讨甲巯咪唑(MMI)对大鼠胃酸分泌以及应激和化学诱导的胃溃疡的影响。使用经MMI(10 - 100 mg/kg,腹腔注射)预处理的幽门结扎大鼠进行胃酸分泌研究。还测试了口服MMI对水浸束缚(WIR)应激、吲哚美辛和乙醇诱导的胃溃疡的影响。在乙醇诱导胃损伤后,测量大鼠腺胃中的髓过氧化物酶(MPO)、非蛋白巯基(NP-SH)水平和胃壁黏液。在接受MMI治疗的大鼠中,胃酸分泌和溃疡原诱导的胃损伤形成受到剂量依赖性抑制。我们的形态学和组织学研究表明,高剂量(100 mg/kg)MMI治疗的大鼠完全预防了乙醇诱导的损伤。在接受MMI治疗的大鼠中,还观察到乙醇诱导的胃MPO活性增加、NP-SH耗竭和胃壁黏液减少明显减轻。这些发现清楚地表明内源性促炎因子和氧化应激参与介导MMI的胃保护作用。

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