缺血预处理第二保护窗对缺血再灌注心肌细胞凋亡和bcl-2的影响

目的 :探讨缺血预处理 (ischemicpreconditioning ,IP)第二保护窗对大鼠缺血再灌注 (ischemia/reperfu sion ,I/R)心肌细胞死亡和凋亡抑制基因bcl 2蛋白和mRNA表达的影响。方法 :采用末端脱氧核苷酸转移酶介导的带萤光的dUTP缺口末端标记 (TUNEL)法以及免疫组织化学和原位杂交方法。结果 :(1)IP组TUNEL法阳性心肌细胞核数量及阳性心肌细胞核占总心肌细胞核数的百分比均明显少于I/R组 (P <0 0 5 ) ;(2 )IP组表达bcl 2蛋白 (mRNA)阳性的心肌细胞数及阳性心肌细胞占心肌细胞总数的百分比均明显高于I/R组 (P <0 0 1)。结论 :(1)IP第二窗能够显著减少大鼠I/R心肌细胞死亡 ;(2 )IP通过上调凋亡抑制基因bcl 2的基因表达可能是其减少大鼠I/R心肌细胞死亡的机制之一

The Effect of the Second Protection Window of Ischemic Preconditioning on Cardiac Myocyte Apoptosis and Expression of Bcl-2 mRNA during Myocardial Ischemia/Reperfusion Course in Rat

Objective: To explore the effect of the second protection window of ischemic preconditioning (IP) on cardiac myocyte apoptosis and bcl-2 expression during myocardial ischemia/reperfusion (I/R) course in rat. Methods: TUNEL,immunohistochemichal and in situ hybridization methods were adopted. Results: 1) The numbers of positive cardiac myocyte nuclear and the percentage of positive cardiac myocyte nuclear in IP group decreased significantly (P<0.05) compared with that of I/R group, respectively; 2) The numbers of bcl-2 protein (mRNA) positive cardiomyocyte and the percentage of protein bcl-2 positive cardiomyocyte in IP group were higher (P<0.01) than those of I/R group, respectively. Conclusions: 1) The second protection window of IP could decrease cardiomyocyte apoptosis significantly. 2) Up-regulating the expression of bcl-2 gene in cardiomyocytes during I/R course may be one of the mechanisms of the second protection window of ischemic preconditioning.