CD151对心肌梗死血流动力学的影响及其信号机制  

Effect of CD151 on hemodynamic variables in rat myocardial infarction model and the signal pathway involved

作　　者：郑振中[1] 刘正湘[2] 王梦洪[1] 郑泽琪[2] 彭景添[1] 魏云锋[1] 

机构地区：[1]南昌大学第一附属医院心血管内科,南昌330006 [2]武汉华中科技大学同济医学院附属同济医院心血管内科

出　　处：《中华急诊医学杂志》2008年第2期153-157,共5页Chinese Journal of Emergency Medicine

基　　金：国家自然科学基金（30570728）;湖北省卫生厅科研基金重点项目（JX2A04）

摘　　要：目的探讨CD151对大鼠心肌梗死模型血流动力学的影响及其分子学机制。方法制作大鼠心肌梗死模型，将携带人CD151基因的重组腺病毒相关病毒（rAAV）载体注入缺血心肌。4周后，心导管测定心脏功能，用逆转录聚合酶链式反应（RT-PCR）检测外源性CD151mRNA的表达，Western blot检测CD151、P13K、Akt的表达。结果心肌梗死后左室功能明显下降，CD151高表达能够明显改善左室功能，并可上调磷脂酰肌醇3-激酶和磷酸化的蛋白激酶B的表达。结论CD151基因的导入能够改善心室功能，其分子机制与P13K／Akt信号通路的激活有关。Objective To investigate the effects of CD151 gene diversely on hemodynamic variables in rat myocardial infarction and the signal pathway involved. Method Rat model of myocardial infarction was formed by ligation of the anterior descending coronary artery and rAAV-CD151 was implanted into the ischemic myocardium, Four weeks after coronary artery ligation, hemodynamic variables were monitored. Exogenous human CD151 mRNA was detected using RT-PCR, and Western blot analysis for CDI51, phosphatidyl inositol 3-kinase （PI3K）, total protein kinase B （Akt）, phospho-Akt （p-Akt） were performed. Results The cardiac function in AMI was markedly deteriorated. Excessive expression of CD151 could significantly improved the hemodynamic variables after myocardial infarction. In addition, CD151 up-regulated the expression of PI3K and p-Akt. Conclusions This study suggests that CD151 improves hemodynamics after myocardial infarction in rats. The molecular mechanism may be associated with activation of PI3K/Akt.

关 键 词：CD151 心肌梗死 血流动力学 磷脂酰肌醇3-激酶 蛋白激酶B 

分 类 号：R542.22[医药卫生—心血管疾病]