局灶性脑缺血再灌注损伤细胞凋亡相关基因表达的研究

A Study on Genes Expression Related to Neuron Apoptosis in the Focal Cerebral Ischemia and Reperfusion Models

目的探讨在局灶性脑缺血再灌注损伤中神经细胞凋亡及相关基因表达的影响及脑缺血后神经细胞凋亡的调控机制。方法利用大鼠局灶性脑缺血再灌注模型,采用免疫组化和逆转录聚合酶链(RT-PCR)反应方法分别检测脑缺血再灌注不同时间细胞凋亡及相关基因bcl-2和bax、Caspase-3表达的动态变化。结果轻度脑缺血和再灌注早期,bcl-2表达升高,具有神经保护作用,但重度脑缺血和再灌注后期,其保护作用不足以抑制神经细胞凋亡。Bax表达于神经细胞凋亡时空分布一致,可反映缺血后脑损伤的程度。Caspase-3在脑缺血再灌注损伤中起重要作用,其表达的升高早于细胞凋亡,直接参与神经细胞凋亡的执行。结论脑缺血再灌注能够引起Bcl-2基因和Caspase-3基因表达的改变,导致神经细胞凋亡的发生。

Objective To investigate neuron apoptosis and the expression of related gene during the focal cerebral ischemia and reperfusion injury, and its regulation mechanism. Methods Focal cerebral ischemia and reperfusion model of rats induced by a suture method preferred by Zea Longa was adopted. Immunohistochemistry and RT-PCR technique were used to examining the dynamic expression changes of bcl-2, bax and Caspase-3 at different time following focal cerebral ischemia and reperfusion in rats so as to explore the regulatory mechanism of neuronal apoptosis. Results In the early stage of mild ischemia and reperfusion, the expression of bcl-2 increased. This is important to the cerebral protection. While in the late stage of severe ischemia and reperfusion, its protection was limited to inhibit the neuron apoptosis. The same spatial chronical distribution of Bax expression and apoptotic neuron suggests that Bax can be used to reflect the cerebral damage severity after ischemia. The expression of Caspase-3 increased earlier than the neuron apoptosis, so Caspase-3 is involved directly in the procedure of neuronal apoptosis. Conclusion The changes of expression of bcl-2 and Caspase 3 induced by cerebral ischemia and reperfusion result the neuron apoptosis.