心肌缺血再灌注交界区细胞凋亡促进因子、p53、bcl-2基因动态表达的临床意义  

Clinical significance of Caspase-3, p53, and bcl-2 expressions at boundary area of myocardial ischemia reperfusion

作　　者：杨廷桐[1] 李秀杰[1] 李荣堂[1] 刘玲玲[2] 

机构地区：[1]新乡医学院,河南省新乡市453000 [2]新乡市中心医院

出　　处：《中国综合临床》2007年第2期97-99,共3页Clinical Medicine of China

基　　金：河南省科委攻关科研基金资助（0524410058）

摘　　要：目的探讨缺血再灌注损伤诱导交界区心肌细胞凋亡与细胞凋亡促进因子（caspase-3）、p53、bcl-2基因动态表达的临床意义。方法采用半定量逆转录．聚合酶链反应技术、原位杂交技术、免疫组化技术等，观察家兔心肌缺血／再灌注模型缺血交界区caspase-3 mRNA、p53 mRNA、bcl-2 mRNA动态表达的内在联系。结果①caspase-3 mRNA与心肌细胞凋亡在缺血再灌注损伤4h后开始升高，12h达高峰，二者之间存在明显正相关性（r=0．9286，P〈0．01）。②p53 mRNA于缺血再灌注8h开始升高。bcl-2 mRNA在缺血再灌注8h时开始激活，并持续维持低水平状态。p53 mRNA和bcl-2 mRNA二者的表达之间存在明显的负相关性（r=-0．9648，P〈0．01）。结论caspase-3的激活进一步上调p53表达，二者促进心肌细胞凋亡，进而影响心肌功能。Objective To study clinical significance of myocardial cell apoptosis and caspase-3 activaty and p53, bcl-2 expression on boundary of myocardial ischemia reperfusion. Methods The relation of Caspase-3 mRNA, p53 mRNA, and the bcl-2 mRNA expressions at the boundary area of the myocardial ischemia reperfusion was detected in the myocardial ischemia/reperfusion model of rabbit by semi-RT-PCR and in situ hybridization and immunohistochemistry. Results ① The caspase-3 mRNA and the cell apoptosis began to increase at 4 h after ischemia reperfusion injury and peaked at 12 h, both of which were positively correlated （r = 0.9286, P 〈 0.01）. ② p53 mRNA upregulated at 8 h of ischemia reperfusion injury and bcl-2 mRNA was activated and maintained the low level. The p53 mRNA was significantly negatively correlated with bcl-2 mRNA （r = -0.9648, P 〈 0.01）. Conclusion The activated capase-3 will upregnlate the expression of p53, both of which will promote the myocardial apoptosis and then affect the myocardial function.

关 键 词：缺血再灌注 心肌细胞凋亡 细胞凋亡促进因子mRNA p53 MRNA BCL-2 MRNA 

分 类 号：R54[医药卫生—心血管疾病]