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机构地区:[1]首都医科大学附属北京友谊医院综合科,100050
出 处:《胃肠病学》2008年第3期174-178,共5页Chinese Journal of Gastroenterology
摘 要:背景:很多胃黏膜损伤模型中发现巯基物质含量下降,巯基物质对胃黏膜细胞具有保护作用。目的:探讨巯基物质对小剂量阿司匹林所致胃黏膜损伤的保护作用。方法:80只雄性Sprague-Dawley(SD)大鼠随机分为正常对照组、纯巯基对照组、阿司匹林模型组、巯基预防组、硫糖铝预防组、NaCl治疗对照组、巯基治疗组和硫糖铝治疗组8组。测定黏膜溃疡指数(UI),行大体、组织学和透射电子显微镜观察,测定胃黏膜组织中还原型谷胱甘肽(GSH)、超氧化物歧化酶(SOD)、丙二醛(MDA)、6-酮-前列腺素F1α(6-keto-PGF1α)水平。结果:阿司匹林模型组胃黏膜发生病变,UI与其余各组相比显著升高(P<0.01),GSH、6-keto-PGF1α含量较正常对照组显著降低(P<0.05),MDA含量显著增高(P<0.001)。巯基预防或治疗后,胃黏膜损伤明显减轻,UI显著下降(P<0.001),GSH、6-keto-PGF1α含量显著增高(P<0.05),MDA含量显著降低(P<0.05)。各组SOD含量无显著差异。结论:小剂量阿司匹林可致大鼠胃黏膜损伤,胃黏膜GSH下降可能是其机制之一。外源性GSH具有增强胃黏膜抗氧化作用和细胞保护作用。Background:The level of sulfhydryl is decreased in many models of gastric mucosal lesions, and sulfhydryl has cytoprotection on gastric mucosal cell. Aims: To study protection of sulfhydryl on gastric mucosal lesions induced by low dose aspirin. Methods: Eighty male Sprague-Dawley (SD) rats were randomly divided into eight groups: normal controt group, sulfhydryl control group, aspirin model group, sulfhydryl protection group, sucralfate protection group, NaC1 treatment control group, sulfhydryl treatment group and sucralfate treatment group. Ulcer indexes (UI) were assessed. Macroscopic, histological and transmission electron microscopic changes were observed. Levels of reduced glutathione hormone (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), 6-keto-prostaglandin (PG) F1α of gastric mucosa were measured. Results: Gastric mucosal lesions were observed in aspirin model group, and UI increased significantly than that in the other groups (P〈0.01); compared with normal control group, levels of GSH, 6-keto-PGF1α decreased and level of MDA increased significantly (P〈0.05, P〈0.001). In sulfhydryl protection and sulfhydryl treatment groups, there were amelioration of gastric mucosal lesions, UI decreased significantly (P〈0.001), levels of GSH, 6-keto-PGF1α increased and level of MDA decreased markedly (P all 〈0.05). No significant differences were found in SOD between various groups. Conclusions: Low dose aspirin can induce gastric mucosal lesions, and its mechanism may involve the decrease of GSH in gastric mucosa. Exogenous GSH can enhance the antioxidative effect of gastric mucosa and has cell protective effect.
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