中文摘要：

目的观察重组9型腺相关病毒（recombinant adeno-associated virus serotype 9，rAAV9）携带CaMEK基因转导心肌细胞是否能减轻缺血再灌注损伤诱导的心肌细胞凋亡。方法分离培养sD大鼠心肌细胞，建立I／R模型，rAAV9-CBA-CaMEK转染心肌细胞。实验分组：（1）正常对照组；（2）I／R组；（3）I／R＋rAAV9-CBA-CaMEK组；（4）I／R＋rAAV9-CBA-CaMEK＋PD98059组。Western blot测定心肌细胞ERKl／2磷酸化水平及Caspase-3、Bax蛋白的表达。结果分离培养的原代心肌细胞经鉴定结果阳性，Western blot分析显示rAAV9介导CaMEK基因转染心肌细胞P．ERKl／2的表达高峰时间在第5天，并可减轻缺血再灌注诱导的心肌细胞凋亡，而给予PD98059处理后，这种心肌细胞保护作用消失。结论rAAV9介导的CaMEK基因转染可显著减轻缺血再灌注诱导的心肌细胞凋亡。

英文摘要：

Objective To determine whether recombinant adeno-associated virus serotyoe 9 with CaMEK gene transfeeted on myocardial cells leads to reduce I/R-induced apoptosis. Methods Establish an ischemic/reperfusion（I/R） model of myocardial cells in vitro and the ceils were divided into four experimental groups ： （ 1 ） control group ; （ 2 ） I/R group ; （ 3 ） I/R＋rAAV9-CBA-CaMEK group ; （ 4 ） I/R＋rAAV9-CBA- CaMEK＋PD98059 group, respectively. The P-ERK1/2 and the Caspase-3, Bax were quqntitated by Western blot. Results These data clearly demonstrate that AAV9-mediated CaMEK gene transfected lead to active ERK1/2 and reduce I/R-induced apoptosis notablely. Conclusion rAAV9-mediated CaMEK gene transfected on myocardial cells can reduce I/R-induced apoptosis.