NF-κB、Bcl-2和Bax蛋白在大鼠脑缺血预处理脑组织中的表达及意义

目的探讨核转录因子-κB(NF-κB)、凋亡调控蛋白Bcl-2、Bax在大鼠局灶性脑缺血预处理脑组织中的表达及意义。方法线栓法阻断SD大鼠大脑中动脉建立脑缺血预处理及脑缺血模型。TTC染色法测量脑梗死体积,免疫组织化学方法检测前脑皮质、基底核NF-κB、Bcl-2和Bax蛋白的表达。结果与缺血组相比,预处理缺血组脑梗死体积明显减小(p<0.01),NF-κB蛋白和Bax蛋白表达的细胞数减少(p<0.001),Bcl-2蛋白表达细胞数明显增加(p<0.001)。结论缺血预处理可有效抑制NF-κB的激活并减少神经元的凋亡,Bcl-2蛋白表达增加和Bax蛋白表达下降可能是缺血预处理产生耐受的原因之一。

The Expression and Significance of NF-κB、Bcl-2 and Bax Proteins in Preconditioning Focal Cerebral Ischemia in Rats

Objective To study the expression and significance of nuclear factor-κB(NF-κB), apoptosis- regulation proteins Bcl-2 and Bax in preconditioning focal cerebral ischemia in rats. Methods Middle cerebral artery (MCA) of the SD rats was blocked by suture-occluded method to establish preconditioning cerebral ischemia model and cerebral ischemia model. The volume of cerebral infarction was calculated by TTC staining, the expressions of NF-κB、 Bcl-2 and Bax proteins in procerebrum cortices and basal nuclei of rats were detected by immunohistochemistry. Results The volume of cerebral infarction in preconditioning ischemia group reduced significantly (p<0.01), the cells expressed Bax and NF-κB proteins decresed (p<0.001), the expression of Bcl-2 increased clearly (p<0.001), compared with ischemia group. Conclusion Ischemia preconditioning can suppress the activation of NF-κB effectively and reduce the death of neural cells.The increase of Bcl-2 and decrease of Bax may be one of the reasons that ischemia preconditioning can produce toleration.