SOD、VitC对局灶性脑缺血再灌注大鼠脑组织HSP70基因表达的影响

Effects of superoxide dismutase and Vitamin C on HSP70 gene expression in rats with focal cerebral ischemia followed by reperfusion

目的 探讨超氧化物歧化酶 (SOD)、维生素 C(Vit C)对脑缺血再灌注损伤保护作用及其机制。方法 参照 Zea longa线栓法略加改进建立大鼠局灶脑缺血再灌注模型 ,根据实验需要分为 4组 ,应用免疫组织化学法 ,以生理盐水 (NS)为对照 ,观察 SOD、Vit C对热休克蛋白 70 (HSP70 )基因表达的影响。结果 与对照组相比 ,SOD(80 0 U / 10 0 g)能显著上调大脑皮质、皮质下白质、海马区 HSP70基因的表达 (χ2 检验 ,P<0 .0 5、P<0 .0 1) ,Vit C(2 0 m g/ 10 0 g)不能上调同一区域 HSP70基因的表达 (χ2 检验 ,P >0 .0 5 )。结论 SOD促进缺血再灌注脑组织HSP70基因的表达 ,是 SOD脑保护作用的分子机制之一 ;Vit C不能促进 HSP70基因的表达 ,其脑保护作用与SOD有所不同。 SOD促进 HSP70的表达不是依赖其清除自由基的作用而是存在另一机制。

Objective To investigate the mechanism of the central neuroprotection of SOD and Vitamin C on cerebral ischemia reperfusion injury. Methods The model of focal ischemia reperfusion in rats was established with the suture occluding method invented by Zea Longa and improved properly in our lab. The HSP70 protein expression in rats treated with SOD (800U/100g) or VitC (20mg/100g) before cerebral ischemia reperfussion was observed by immunohistochemical method. Results As compared with the control groups,SOD might increase the expression of HSP70 gene both in the ischemia cerebral cortex and in basal ganglia (χ 2 test,P<0.05),where as VitC,did not. Conclusion Increasing the expression of HSP70 gene may be one of the mechanisms of the central neuroprotection of SOD,but VitC can not increase the expression of HSP70 gene. So it differs from SOD in the effect of neuroprotection.