大鼠局灶性脑缺血Bcl-2和Bax的表达与细胞凋亡

The expression of Bcl-2/Bax and neuron death after focal cerebral ischemia in rat

目的:研究大鼠局灶性脑缺血再灌注后凋亡相关基因Bcl-2和Bax在缺血皮层表达的变化及其与神经元凋亡的关系。方法:线栓法制作大鼠局灶性脑缺血再灌注模型,免疫组化法观察Bcl-2和Bax的表达变化,TUNEL法观察神经元凋亡的情况。结果:再灌注2h后皮层神经元Bcl-2表达开始明显上调,6h为高峰,之后开始下降。再灌注早期 Bax在皮层神经元的表达即明显增强,24～48h达高峰。Bcl-2／Bax的比率在再灌注开始时升高,6h达高峰,随后开始下降。TUNEL阳性细胞主要分布在缺血中心的边缘,再灌注48h之内,随时间的延长而不断增加。结论:Bcl-2／Bax的比率改变与缺血再灌注后的神经元存亡相关。

Objective： The aim of this study was to investigate the change of Bcl-2 / Bax expression and the neuron death in transient focal cerebral ischemia in rat . Methods： Experimental models of focal ischemia were produced by intraluminal occlusion of the middle cerebral artery （MCAO） in rats, using immunohistochemical technique in analyzing the expression of Bcl-2 and Bax. The TUNEL staining method was used to characterise the apoptotic cell death. Results：Our results show that the immunoreactivities of both the antiapoptotic agent Bcl-2 and the proapoptotic agent Bax were upregulated, During reperfusion after 2h of ischemia, the expression of Bcl-2 was induced in the ischemic cortex with peak expression at 6h, and then decreased. The expression of Bax was observed markedly in the ischemic cortex at early stage of reperfusion, lmmunoreactivity of Bax increased with time after reperfusion with peak expression at 24-48h. The ratio of Bcl-2/ Bax increased at the beginning of reperfusion with peak at 6h, decreasing in the following time. The TUNEL-posirive cells were more apparent in the inner border regions immediately adjacent to the ischemic core and progressively increased at 48h. Conclusion： This demonstrates that a specific alteration of the Bax/Bcl-2 ratio would play a vital role in regulating the neuronal survival or death during transient focal cerebral ischemia.