氯化亚锡对大鼠肾缺血再灌注损伤的作用和血红素氧合酶-1表达的影响

Protective effect of induced heme oxygenase-1 by SnCl_2 on renal ischemia and reperfusion injury in rats

目的:探讨氯化亚锡(SnCl2)对大鼠肾急性缺血再灌注损伤的改善作用和血红素氧合酶-1(HO-1)表达的影响。方法:建立大鼠肾缺血再灌注模型,随机将动物分为假手术组、对照组及实验组。实验组在肾脏缺血前24h皮下注射SnCl2100mg/kg,肾脏缺血45min再灌注24h后切取肾脏,分别应用免疫组织化学及双抗夹心ELISA检测HO-1蛋白的表达,并测定肾组织中超氧化物岐化酶(SOD)的活性及丙二醛(MDA)的含量。同时测定血尿素氮(BUN)、肌酐(Cr)水平。结果:对照组缺血再灌注前后血Cr、BUN水平、SOD活性及MDA含量差异均有统计学意义(P<0.05),而假手术组、实验组差异均无统计学意义(P>0.05)。假手术组、对照组及实验组大鼠肾组织匀浆中HO-1含量依次增高(P<0.05)。结论:应用SnCl2预处理诱导HO-1的表达可通过清除氧自由基的毒性作用而减轻大鼠肾缺血再灌注损伤。

Aim ： To investigate the protective effect of heme oxygenase-1 （ HO-1 ） induced by SnCl2 on renal ischemia and reperfusion injury in rats. Methods： A total of 48 Wistar rats were allocated into sham-operation, model control group and experimental group randomly. In the experimental group, SnCl2 was administered subcutaneously at 24 h prior to the renal artery clamp for 45 min in order to prepare the ischemia model. After 24 h reperfusion, the kidney was removed to detect the levels of HO-1 using immunohistochemistry and double antibody capture ELISA, respectively. SOD activity and MDA content in the renal tissue were examined. The renal function was also assessed by determining the levels of blood urea nitrogen（BUN） and serum creatinine （ Cr）. Results ： HO-1 levels increased in sequence of sham-operation group, control group,and experimental group（ P 〈 0.05 ）. There were significant differences in BUN, Cr, SOD activity and MDA before and after reperfusionin in control group（ P 〈 0.05 ） , but not in sham-operation and experimental group（ P 〉 0.05 ）. Conclusion： Pretreated renal tissue with SnCl2 can induce HO-1 that can reduce ischemia reperfusion injury through the way of scavenging the toxic free radicals.