还原型谷胱甘肽对缺氧/复氧培养大鼠心肌细胞的干预性研究  

Reduced glutathione protects against anoxia/reoxygenation injury of cultured myocardial cells in rats

作　　者：赵丽丽[1] 王一彪[1] 朱晓波[1] 张兆华[1] 

机构地区：[1]山东大学第二医院儿科,山东济南250033

出　　处：《山东大学学报（医学版）》2005年第11期1049-1051,1054,共4页Journal of Shandong University:Health Sciences

摘　　要：目的:探讨还原型谷胱甘肽(GSH)对缺氧/复氧培养大鼠心肌细胞损伤的保护作用。方法:将原代培养的乳鼠心室肌细胞分为正常对照与GSH不同浓度处理组,缺氧、复氧前均给予0、40、80、160mg/L浓度的GSH,缺氧2h,复氧1h。应用黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活性,用硫代巴比妥酚显色法测定丙二醛(MDA)含量。结果:与对照组相比,单纯缺氧/复氧(0mg/L)组SOD活性显著下降、MDA水平显著升高(P<0.01)。GSH预处理以剂量依赖性减轻细胞活力下降及MDA的上升,而对SOD的作用则在160mg/L组达到峰值。结论:GSH对缺氧/复氧损伤的心肌细胞具有保护作用,其机制可能与GSH的抗氧化作用有关。Objective：To investigate the protective effect of reduced glutathione sodium （GSH） on anoxia/reoxygenation injury of myocardial cells in rats. Methods： Primary cultured myocardial cells of rats were randomly allocated to control group and GSH groups which were respectively given 0,40,80,160 mg/L GSH before 2-hour anoxia or 1-hour reoxygenation. Before anoxiated, at 2 hours after anoxiated, and at 1 hour after reoxygenated, the activities of superoxide dismutase （SOD） were measured by the method of xanthine oxidase, and the contents of serum malonicaldehyde（MDA） were determined by the method of thiobarbituric acid. Results：Compared with control, the activity of SOD was markedly decreased,while the content of cellular MDA was significantly increased in 0 mg/L GSH of anoxia/reoxygenation group （P〈0.01）. GSH in a dose-dependent manner could significantly decrease the reduced SOD activity and the ascending MDA,and GSH in 160 mg/L had the greatest protective effect on SOD. Conclusion：GSH protects the myocardial cell from anoxia/reoxygenation injury, which may be related to the ability of GSH in against oxidant injury.

关 键 词：缺氧 复氧 心肌 还原型谷胱甘肽 大鼠 WISTAR 

分 类 号：R365.54[医药卫生—病理学] R-33[医药卫生—基础医学]