热休克蛋白32对脑缺血再灌注损伤大鼠脑组织抗氧化能力的影响

摘要

Objective To investigate the antioxidant effect of heat shock protein 32(HSP32) on focal cerebral ischemia-reperfusion injury in rats. Methods Thirty-six male SD rats of clean grade weighing 220 - 250g were randomly divided into 3 groups ( n = 12 in each group) :sham operation group(S group) .ischemia and reperfusion group (IR group) ,and Znpp group(Z group). The focal cerebral ischemia-reperfusion model was established using nylon suture method of the right internal carotid artery to induce the middle cerebral artery occlusion. In Znpp group,the inhibitor of HSP32 Znpp 45 u,mol/kg was intraperitoneally injected in rats. All rats were sacrificed after 6 h reperfusion. Light microscope was used to observe the pathological changes of brain tissue. SOD activity, MDA content and HSP32 protein expression were detected in brain tissues. Results Compared with sham group,MDA significantly increased and SOD significantly decreased in the other two groups(P < 0.05). There was no significant difference in HSP32 expression between sham group and Znpp group (P>0.05) , while HSP32 expression was significantly higher in IR group than those in the other groups{P < 0.05 ). Compared with IR group, MDA significantly increased and SOD significantly decreased in Znpp group(P < 0.05 ). Conclusion Cerebral ischemia and reperfusion can induce the expression of heat shock protein 32 to reduce the oxidative damage after reperfusion.%目的 探讨热休克蛋白32( HSP32)在局灶性脑缺血再灌注损伤中的抗氧化作用. 方法 将36只清洁级雄性SD大鼠随机分为3组,每组12只:假手术组(S组)、缺血再灌注组(IR组)和锌原卟啉IX(Znpp)+缺血再灌注组(Z组).采用右侧颈内动脉尼龙线线栓法致大脑中动脉栓塞法制备局灶性脑缺血再灌注模型.Z组在造模前经腹腔注射HSP32特异性抑制剂Znpp(45 μmol/kg).所有大鼠再灌注6h后处死取脑,光镜下观察各组脑组织病理变化,检测脑组织中SOD活性、MDA含量和HSP32蛋白表达. 结果 与S组比,IR组和S组SOD显著降低(P＜0.05),MDA显著升高(P＜0.05)；IR组HSP32蛋白的表达显著增多(P＜0.05),Z组HSP32的表达与S组差异无统计学意义(P＞0.05)；与IR组比,Z组MDA显著升高(P＜0.05),SOD显著降低(P＜0.05). 结论 脑缺血再灌注可以诱导热休克蛋白32的表达,使再灌注后的氧化损伤减轻.