Bcl-2对脑缺血再灌注后神经元DNA的自我保护作用

The effect of Bcl-2protection on neu ronal DNA damage after cerebral isch emia and reperfusion

目的研究脑缺血再灌注(IR)后神经元DNA损伤及Bcl-2的调控作用。方法制作局灶性IR模型,按再灌注时间分6组,检测不同时相缺血区神经元DNA损伤、Bcl-2表达变化和MDA含量。结果IR后6h,TUNEL阳性细胞数升高,24h达高峰,72h仍有较强表达;Bcl-2表达IR后1h升高,6h达高峰,72h趋于阴性;IR后1h,丙二醛(MDA)含量显著升高,6～12h后恢复假手术组水平,24h又出现增高。脑组织DNA损伤与Bcl-2表达呈显著负相关。结论Bcl-2通过抑制氧自由基的产生而减少神经元DNA损伤,具有神经元自我保护作用,提高了神经元的存活率。

Objective To investigate neuronal DNA damage a nd the regulation of Bcl-2after cere bral ischemia and reperfusion.Methods By using the model of focal cerebral i schemia and reperfusion,DNA damage,Bcl-2expression,MDA content were examined at different hours after reperfusion.Results TUNEL positive cells began to rise fr om 6h after reperfusion,reached peak at 24h and became rehabilitated gradually after 72h in ischemic brain tissue.Bcl-2expression increase d at 1h after reperfusion,reached peak at 6h,reduced at 24h and re-turned to normal level by 72h after re perfusion.MDA content in ischemic b rain issue began to increase at 1h after reperfusion,returned to FO level during 6～12h and reached anoth er high mark at 24h after reperfusion.A significantly negative correlation existed between neuronal DNA damage and Bcl-2expression(P<0.05).Conclusions This indicates that Bcl-2may reduce neuronal DNA damage and protect neu-rons by restraining oxygen free radi cals.