Bcl-2和Bax在缺血预处理保护海马神经元缺血再灌损伤中的作用

The role of bcl-2 and bax in the protection of hippocampal neurons by cerebral ischemic preconditioning against ischemia/reperfusion injury

目的:探讨凋亡相关基因bcl-2和bax在缺血预处理(ischemic preconditioning,IPC)保护大鼠海马神经元缺血再灌损伤中的作用。方法:随机将动物分为IPC加缺血再灌组(IPC组)、单纯缺血再灌组(IR组)和对照组。观察海马CA1区神经元的组织形态学变化;TUNEL染色检测海马CA1区神经元凋亡;免疫组化测定海马CA1区神经元Bcl-2和Bax的表达。结果:IPC组海马CA1区神经元存活数显著多于IR组,凋亡细胞数显著低于IR组,Bcl-2呈强表达,Bax表达不明显。结论:IPC诱导Bcl-2表达上调和Bax蛋白表达下调,可抑制凋亡的发生,对海马CA1区神经元缺血再灌损伤起保护作用。

Objective： To investigate the role of apoptotic related genes, bcl-2 and bax in the protection of hippocampal neurons by cerebral ischemic preconditioning （IPC） against ischemia/reperfusion injury in rats. Methods： Rats were randomly divided into ischemic preconditioning ＋ ischemia reperfusion group （IPC）, ischemia/ reperfnsion group （IR）,and control group. Histological changes in the neurons of the hippocampal CA1 region were observed. The apoptosis of neurons in hippocampal CA1 area was determined by TUNEL staining. The expression of Bcl-2 and Bax was detected with immunohistochemistry. Results： Cerebral ischemic preconditioning may increase the number of alive neurons in hippocampal CA1 region（ P 〈 0.05）, markedly reduce the apoptosis of pyramidal neurons （ P 〈 0.05）, and induce the expression of Bcl-2 and inhibit the expression of Bax（ P 〈 0.05）. Conclusion： Cerebral ischemic preconditioning （IPC） inducing upregulation of Bcl-2 expression and downregulation of Bax expression may inhibit the apoptosis and protect the hippocampal neurons against ischemia/reperfusion injury.