自噬在米诺环素保护肾缺血再灌注损伤中的作用

Minocycline attenuates renal ischemia-reperfusion injury by inducing autophagy

目的:研究米诺环素对肾缺血再灌注损伤后自噬的影响,探讨自噬在米诺环素保护肾缺血再灌注损伤中的作用。方法:建立大鼠肾缺血再灌注损伤模型,采用米诺环素及自噬抑制剂干预,观察大鼠肾脏指数、肾功能变化;HE染色评价肾组织病理学变化;Western blot法检测肾组织自噬相关蛋白LC3、Beclin 1、p62的表达。结果:米诺环素可以显著改善肾缺血再灌注损伤后的肾脏损伤,而自噬抑制剂氯喹能部分逆转米诺环素的肾保护作用。Western blot结果显示,米诺环素可上调缺血再灌注损伤肾组织LC3并下调p62的表达水平,而氯喹能部分逆转米诺环素的自噬诱导作用。结论:米诺环素对肾缺血再灌注损伤具有显著的保护作用,其机制可能是通过激活自噬实现的。

AIM： To investigate the role of autophagy in the renal ischemia-reperfusion injury treatment with minocycline. METHODS： Rat models of renal ischemia-reperfusion injury were established, then treated with minocycline and chloroquine. Renal index, renal function and renal morphological features were observed. The expression of autophagy-related proteins including LC3, Beclin 1 and p62 were examined by Western blot. RESULTS ：Minocycline remarkably decreased the renal ischemia-reperfusion injury, and inhibition of autophagy with ehloroquine partly reversed the renoprotective effect of minocycline. Western blot showed that minocycline up-regulated LC3 and down-regulated p62 protein expression. Chloroquine partly reversed the autophagy induced by minocycline. CONCLUSION： Minocycline can protect the kidney against ischemia-reperfusion injury in rats, and one of the mechanism maybe realized by inducing autophagy.