缺血再灌注心肌细胞Caspase-3/Bcl-2表达与细胞凋亡的关系

Caspase-3/Bcl-2 Expression and Cell Apoptosis in Ischemia-reperfusion Myocardial Cells

目的:探讨Caspase-3/Bcl-2基因的动态表达与缺血再灌注(IR)心肌细胞凋亡的关系。方法:建立家兔心肌IR模型,采用原位杂交、免疫组化等技术,观察IR后Caspase-3及Bcl-2 mRNA的动态表达规律与心肌凋亡细胞数目的关系。结果:(1)Caspase-3与细胞凋亡的发生呈正相关性(r=0.9286,P<0.001);(2)Caspase-3与Bcl-2之间形成一种抗衡的网络调控构象,负责凋亡的促进和凋亡的抑制;(3)Caspase-3、Bcl-2 mRNA与细胞凋亡三者的表达在交界区比梗死区更明显。结论:Caspase-3活化诱导的细胞凋亡是IR引起心肌细胞损伤的主要原因;交界区的细胞凋亡是IR损伤的主要标志。

Objective： To explore the relationship of Caspase-3 activate and expression of the Bcl-2 genes with the apoptosis of ischemia reperfusion in myocardial cell. Methods： The models of myocardial ischemia/reperfusion in rabbit were established The expression of Caspase-3 mRNA and Bcl-2 mRNA were measured in different time of IR by hybridizafion in sire. and the apoptosis of myocardial cell was measured at the samc time, and then their relationship was analyzed. Result： （1）lscbemia/reperfusion injury to stir up the caspase-3 to activate, promote the apoptosis take place, two curve varieties present the positive relativity.（r=0.9286, P〈0.001）. （2）Capase-3, Bcl-2 were a kind of to match of network adjust to control, be responsible for the apoptosis promote to repress. （3）The expressions of capase-3 mRNA.Bcl-2 mRNA,apoptosis, at the boundary area more obvious than the infarct area Conelusions： Caspase-3 activation of IR-reduced cell apoptosis is the main cause of myocardial cell injury; junction cell apoptosis is the main mark of IR injur.