大鼠局灶性脑缺血再灌注后海马Bcl-2、Bax蛋白的表达

目的 探讨大鼠局灶性脑缺血再灌注后Bcl-2、Bax蛋白在海马表达的变化.方法 线栓法制作大鼠局灶性脑缺血再灌注模型,应用免疫组化染色检测Bcl-2、Bax蛋白表达,应用TUNEL法检测海马区细胞凋亡.结果 缺血再灌注2h后海马神经元Bcl-2、Bax蛋白开始表达,Bcl-2蛋白12h达高峰,Bax蛋白12h～24h达高峰,之后开始下降.再灌注2h后海马凋亡细胞开始表达,随着再灌注时间的延长,其表达不断增加.Bcl-2/ Bax的比率在再灌注开始时升高,再灌注12h达高峰,随后开始下降.结论 凋亡是脑缺血再灌注损伤的重要形式之一,Bcl-2/ Bax的改变与缺血再灌注后海马的神经元存亡有关,缺血再灌注可导致海马神经元凋亡.

The expression of Bcl-2 and Bax after focal cerebral ischemia-reperfusion in rats

Objective To study the change of Bcl-2 and Bax expression following focal cerebral ischemia-reperfusion in rats.Methods The focal cerebral ischemia-reperfusion model was made by thread embolisk of middle cerebral artery(MCA).Immunohistochemical technique was used to analyze the expression of Bcl-2 and Bax.Results During reperfusion after 2h of ischemia,the expression of Bcl-2 was induced in the ischemic hippocampus with peak expression at 12h,and then decreased.The expression of Bax was observed markedly in the ischemic hippocampus at early stage of reperfusion.Immunoreactivity of Bax increased with time after reperfusion with peak expression eluring 12-24h.During reperfusion after 2hours of ischemia,the expression of apoptosis cell was induced in the ischemic hippocampus,and then decreased.The ratio of Bcl-2/Bax increased at the beginning of reperfusion with peak at 12hs,decreasing in the following time.Conclusion The change of Bcl-2/Bax ratio would play a vital role in regulating the neuronal survival or death during reperfusion after focal cerebral ischemia.