摘要
目的:在家兔急性心肌梗死模型中观察缺血后处理对家兔心肌窦房结细胞缺血再灌注(IR)的作用及Bcl-2和Bax蛋白表达的影响。方法:在体成年家兔右冠状动脉缺血再灌注模型分4组:正常对照组、IR组、缺血预处理(IPC)组、缺血后处理组。观察缺血后处理对家兔在体窦房结细胞IR损伤及Bcl-2和Bax蛋白表达的变化。结果:对照组细胞凋亡、Bcl-2和Bax蛋白表达极少;IPC、缺血后处理组较IR组窦房结细胞凋亡数目显著减少,Bcl-2蛋白表达显著增强,Bax蛋白表达显著减弱;IPC组与缺血后处理组细胞凋亡数目、Bcl-2和Bax蛋白表达无显著差异。结论:IR损伤可诱导窦房结细胞凋亡,IPC、缺血后处理可通过提高Bcl-2蛋白表达同时下调Bax蛋白表达水平从而减少窦房结细胞凋亡,但两组干预效果无明显差异。
Objective： To observe the effects of ischemic postconditioning on the sinoatrial node cell ischemia reperfusion（IR） of rabbits in body and the expression of Bcl-2 and Bax protein in acute myocardial infarction models of rabbits. Methods：The ischemia-reperfusion models of the right coronary artery of adult rabbits in body were randomly divided into a normal control group,an IR group, an ischemic preconditioning group（IPC） and an ischemic postconditioning group to observe the injury of ischemic postconditioning on the sinoatrial node cell ischemia reperfusion （IR） and the changes of Bcl-2 and Bax protein expression in rabbits in body. Results：The cell apoptosis,the Bcl-2 and Bax protein expression were very few in the control group. Compared with the IR group,the numbers of the sinoatrial node cell apoptosis were reduced significantly, the Bcl-2 protein expression was increased significantly and the Bax protein expression was attenuated signifi cantly in the IPC group and the ischemic postconditioning group. The cell apoptosis numbers, the Bcl-2 and Bax protein expression in the IPC group and the ischemic postconditioning group had no significant difference. Conclusions： IR injury may induce the apoptosis of the sinoatrial node cell. The IPC and the ischemic postconditioning may decrease the Bax protein expression by increasing the Bcl-2 protein expression so as to reduce the sinoatrial node cell apoptosis,but there is no significant difference in the intervention effect between the two groups.
出处
《山西职工医学院学报》
CAS
2009年第1期1-3,共3页
Journal of Shanxi Medical College for Continuing Education
关键词
窦房结
缺血再灌注
缺血预处理
缺血后处理
凋亡
sinoatrial node
ischemia reperfusion
ischemic preconditioning
ischemic postconditioning
apoptosis
