【摘要】 [目的]探讨缺血后处理对大鼠肾缺血再灌注损伤影响。[方法]夹闭左侧肾动脉60 min后再灌注6 h法制备肾脏缺血再灌注损伤模型。雄性SD大鼠18只随机分为3组:缺血再灌注组(IR组,n=6),缺血后处理组(IPO组,n=6),假手术组(Sham组,n=6)。测定血肌酐(Cr)浓度、尿素氮(Bun),检测肾脏组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量和髓过氧化物酶(MPO)活性;取左肾组织行HE染色,光镜下观察肾组织病理学改变,免疫组化法检测肾组织中NF-κB表达。[结果]与Sham组比较,IR组血Cr浓度和血Bun浓度上升,达到(93.02±13.44)μmol/L和(15.58±0.56)mmol/L(P<0.01),SOD活性下降为(185.87±17.68)U/mgprot(P<0.01),MDA含量和MPO活性增加分别达到(4.09±0.34)nmol/mgprot、(0.90±0.07)U/g(P<0.01)。与Sham组比较IPO组血Cr、Bun浓度、MPO活性差异有统计学意义(P<0.05),SOD活性和MDA含量差异无统计学意义;病理损伤明显,肾脏组织中NF-κB表达增强。与IR组比较,IPO组血Cr和血Bun浓度降低分别为(58.98±8.02)μmol/L(P<0.01)、(9.45±1.03)mmol/L(P<0.01),SOD活性升高为(230.90±9.19)U/mgprot(P<0.01),MDA含量降低为(3.67±0.20)nmol/mgprot(P<0.01),MPO活力降低为(0.78±0.06)U/g(P<0.01),病理损伤减轻,肾脏组织NF-κB表达减弱。[结论]缺血后处理对肾脏有保护作用,其机制与增强肾脏抗氧化能力,减轻肾脏组织炎性细胞浸润和抑制肾组织NF-κB表达有关。更多还原

【Abstract】 [Objective] To investigate the effects of ischemic postconditioning on the ischemia-reperfusion injury in rat kidney.[Methods]Eighteen male SD rats were randomly divided into three groups as follows:(1)IR group(n=6).(2)Ischemic postconditioning group(n=6)(3)Sham group(n=6): Rats underwent the same surgical procedure without obstruction for 1 h.At the end of reperfusion for 6 h,the blood urea nitrogen(Bun),blood creatinine concentrations(Cr)were measured,the ischemic left renal tissue was collected for the determination of the superoxide dismutase(SOD) activity,malondialdehyde(MDA)content,myeloperoxidase(MPO) activity and the expression of NF-κB;the changes of renal tissue were observed by microscope.[Results] The Bun,Cr,MPO activity were significantly higher in IR and IPO group than those in Sham group(P<0.05).SOD activity was lower whereas the MDA content was higher in IR group than those inSham group(P<0.05) and the expression of NF-κB in IR group was significantly stronger than that in Sham group.In IPO group the Bun,Cr,MDA and MPO were significantly lower whereas SOD activity was significantly higher(P<0.01) than those in IR group(P<0.05),the expression of NF-κB was weaker than that in IR group.[Conclusion]Ischemic postconditioning attenuates renal ischemia-reperfusiong injury in rats.The mechanism is related to the enhancement of renal tissue antioxidation,inhibite of the neutrophilinfiltration and of NF-κB expression.更多还原