阿托伐他汀早期干预对急性心肌梗死心肌细胞凋亡的影响  

The effect of early atorvastatin therapy on cardiomyocyte apoptosis and its primary mechanisms in rabbit's acute myocardial infarction

作　　者：刘军[1] 夏勇[1] 李东野[1] 陈清枝[1] 

机构地区：[1]徐州医学院附属医院心内科,江苏省221002

出　　处：《中国心血管病研究》2007年第4期292-295,共4页Chinese Journal of Cardiovascular Research

基　　金：江苏省社会发展科研项目资助课题(BS20020009);江苏省高校省级重点实验室开放课题(KJS04006)

摘　　要：目的探讨不同剂量阿托伐他汀提早干预治疗,对兔急性心肌梗死(AMI)细胞凋亡的影响。方法24只新西兰兔随机分为3组:①对照组:不予药物干预;②低剂量组:0.5mg·kg-1·d-1阿托伐他汀;③高剂量组:5mg·kg-1·d-1阿托伐他汀。在药物干预3d后制作AMI模型,检测心肌梗死及其边缘区细胞凋亡率并观察心肌Bax和Bcl-2表达。结果①高剂量组心肌细胞凋亡率明显低于对照组和低剂量组(P<0.05,P<0.01)。②高剂量组Bcl-2表达高于对照组及低剂量组(P<0.01,P<0.05),对照组与低剂量组差异无统计学意义;三组Bax表达均较高,但组间比较,差异无统计学意义。③Pearson线性相关分析显示梗死及其边缘区心肌细胞凋亡率与相应区域Bcl-2表达呈负相关,与心肌组织Bax表达无明显相关关系。结论高剂量阿托伐他汀降低梗死区及其边缘区心肌细胞凋亡率,与低剂量相比显示出更好保护作用。Objective To investigate the effects of different doses of atorvastatin on cardiomyocyte apoptosis and primary mechanisms in the early phase of acute myocardial infarction（AMI）. Methods 24 New Zealand rabbits were randomly separated into three groups： the control group （n=8）treated without lipid-lowering drugs, 0.5 mg·kg^-1·d^-1（n=8）and 5 mg·kg^-1·d^-1（n=8）atorvastatin groups with 3 days of treatments.Then,the model of AMI was established by coronary-occluded method,and six hours later,myocardial apoptotic rate and the expression of Bax,Bcl-2 were detected. Results （1）To compared with control and 0.5 mg·kg^-1·d^-1 atorvastatin groups, the apoptotic rate in 5 mg·kg^-1·d^-1atorvastatin group significantly lowered（P〈0.05 and P〈0.01 respectively ）, while no significant differences was observed in the control and 0.5 mg·kg^-1·d^-1 atorvastatin group. （2）Both Bax and Bcl-2 expressed in cytoplasm. The content of Bax had no changes in every group, while that of Bcl-2 was evidently in creased in 5 mg·kg^-1·d^-1 atorvastatin group than control and 0.5 mg·kg^-1·d^-1 atorvastatin group in both infarcted and border zone. （3）Correlation analysis indicated that there was a negative correlation between the rate of cardiomyocytes apoptosis and Bcl-2 expression,while there were no relation between the apeptotic rate and Bax by pearson correlation analysis. Conclusion Early intensive atorvastatin intervention may decrease cardiomyocyte apoptosis. Atorvastatin may be through pro-expression of Bcl-2 to resist apoptosis. Early intensive atorvastatin treatment may yield more significant benefits in AMI.

关 键 词：阿托伐他汀 心肌梗塞 凋亡 基因 BCL-2 基因 Bax 

分 类 号：R542.22[医药卫生—心血管疾病] Q95-33[医药卫生—内科学]