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

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

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。

Objective To study the expression and significance of nuclear factor- kB（NF- kB）, 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 TI＇C staining, the expressions of NF-kB, 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- kB 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- kB 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.