富氢盐水对肾脏缺血再灌注损伤的保护作用机制

Protective mechanisms of hydrogen rich saline on renal ischemia-reperfusion injury

目的探讨富氢盐水对肾脏缺血再灌注损伤的保护作用机制。方法将小鼠分为对照(假手术)组,缺血再灌注(IR)组,缺血再灌注+富氢盐水处理(IR+HRS)组。IR+HRS组小鼠于手术前3d及再灌注前1min尾静脉注射0.2mL HRS,再灌注后的2h内每隔0.5h注射1次HRS,对照组和IR组给予相同剂量和频率的生理盐水。手术后24h检测血清肌酐(SCr)和尿素氮(BUN)水平,肾脏组织超氧化物歧化酶(SOD)和丙二醛(MDA)水平及Bcl-xl,Bcl2,Bak,Bax,Cleaved Caspase-3蛋白表达水平。结果 HRS处理能够降低小鼠血清SCr和BUN水平,降低肾脏MDA水平,降低促凋亡蛋白Bak,Bax,Cleaved Caspase-3表达水平;提高肾脏SOD酶活性及抗凋亡蛋白Bcl-xl,Bcl2表达水平。结论 HRS通过清除肾脏氧自由基,提高抗氧化能力及调节细胞凋亡信号通路发挥对肾脏缺血再灌注损伤的保护作用。

Objective To explore the protective mechanisms of hydrogen-rich saline on renal ischemia-reperfusion injury.Methods Mice were divided in to 3 groups:control(sham operation),ischemia-reperfusion(IR)and ischemia-reperfusion+hydrogen-rich saline(HRS).Mice in IR+HRS group were administrated HRS by intravenous injection 3days and 1min before operation and 4 times in the following 2hours after operation.Mice in control and IR group were administrated normal saline as the same volume and frequency with IR+HRS group.Mice were sacrificed 24 hours after operation,creatinine and urea nitrogen in serum were detected by biochemical analyzer,MDA and SOD level were detected by spectrophotometer,expression of Bcl-xl,Bcl2,Bak,Bax,Cleaved Caspase-3 proteins level were detected by western blot.Results Compared to IR group,creatinine,urea nitrogen,MDA level decreased significantly after HRS consumption.SOD enzyme activity increased significantly after HRS consumption.HRS treatment down-regulates expression of Bak,Bax and Cleaved Caspase-3 protein level,and up-regulates expression of Bcl2,and Bcl-xl protein level.Conclusion HRS eliminates ROS and elevates antioxidant activity in renal after IR,besides,HRS also regulate apoptosis signal pathway to protect IR injury in renal.