急性缺血-再灌注肾损伤小鼠肾组织Caspase-1蛋白表达及酶活性变化

目的探讨急性缺血-再灌注肾损伤时caspase-1蛋白表达及酶活性变化。方法复制急性缺血-再灌注肾损伤小鼠模型,应用全自动生化分析仪测定血尿素氮(BUN)及血清肌酐(Scr)水平,应用免疫组化及荧光标记法分别测定肾组织caspase-1蛋白表达水平以及其酶活性的变化。结果模型组Scr和BUN水平均较假模组显著升高;模型组肾组织caspase-1表达强度较假模组显著升高;模型组肾组织caspase-1酶活性也较假模组显著升高。结论Caspase-1产生及活性升高参与急性缺血-再灌注肾损伤,抑制该酶活性,从而控制其下游炎症因子的过度活化可能对肾脏急性缺血-再灌注具有保护作用。

Expression of caspase-1 and its enzymatic activity in acute ischemia-reperfusion injured kidney in mice

Objective To investigate the changes of caspase-1 expression and its enzymatic activ- ity during acute renal ischemia-reperfusion injury. Methods Mice model of acute renal ischemia-reperfusion injury was established. Serum creatinin (Scr) and blood urea nitrogen (BUN) were measured by an auto- analyzer. Caspase-1 expressed in renal tissue was detected by immunohistochemistry, and the enzymatic activity of caspase-1 was measured by a fluorescent microplate reader. Results Scr and BUN were increased significantly in the group of acute renal ischemia-reperfusion injury as compared with those in the control group treated with sham operation. Caspase-1 expression and its activity in renal tissue were also much higher in acute renal ischemia-reperfusion injury model than in the controls. Conclusion The over expression and activation of caspase-1 in renal tissue may play an important role in the pathogenesis of acute renal ischemic- reperfusion injury. Control of the hyperactive downstream cytokine network through the inhibition of caspase-1 activity may be a new strategy for the therapy of acute renal ischemia-reperfusion injury.