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目的 探讨表没食子儿茶素没食子酸酯 (EGCG)对大鼠肾缺血再灌注损伤的影响。方法 通过结扎肾动脉 60min后再灌注 ,建立大鼠肾缺血再灌注损伤模型 ,给药组于结扎前后分别静脉给予 10mg·kg-1和 40mg·kg-1EGCG。化学法观察大鼠血清肌酐 (Scr)、尿素氮 (Bun)、丙二醛(MDA)含量 ,肾组织内MDA、活性氧 (ROS)含量和超氧化物歧化酶 (SOD)、Ca2 + ATP酶活性的变化 ,并观察肾组织的病理变化。结果 与模型对照组比较 ,40mg·kg-1的EGCG组可抑制由肾缺血再灌注引起的血清Bun、Scr、MDA含量和组织MDA、ROS含量的变化 ,增强SOD和Ca2 + ATP酶活性 ,减轻肾组织病理改变。结论 EGCG有保护大鼠肾缺血再灌注损伤的作用 ,其机制可能与抗自由基损伤和减少细胞内钙有关
Objective To investigate the effects of epigallocatechin gallate (EGCG) on renal ischemia-reperfusion injury in rats. Methods Rat kidney ischemia-reperfusion injury model was established by ligating the renal artery for 60 min after reperfusion. The administration group received intravenous administration of 10 mg·kg-1 and 40 mg·kg-1 EGCG before and after ligation, respectively. The serum creatinine (Scr), urea nitrogen (Bun) and malondialdehyde (MDA) levels were measured by chemical methods. The contents of MDA, reactive oxygen species (ROS), superoxide dismutase (SOD) and Ca2 + ATPase in renal tissue were observed. Changes in activity and observation of pathological changes in kidney tissue. Results Compared with the model control group, the 40 mg·kg-1 EGCG group could inhibit the changes of serum Bun, Scr, MDA contents, MDA and ROS contents in the tissues caused by renal ischemia-reperfusion, and increase the activity of SOD and Ca2 + ATPase. Reduce renal pathological changes. Conclusion EGCG can protect renal ischemia-reperfusion injury in rats. The mechanism may be related to anti-free radical damage and reduction of intracellular calcium.