压力超负荷下bcl-2、bax蛋白对兔左室细胞凋亡的影响

Effect of bcl-2 Protein and Bax Protein Expression on Mytocyte Apoptosis During Chronic Pressure Overload in Left Ventricle of Rabbit

目的探讨压力超负荷时兔左室心肌细胞bcl 2和bax蛋白表达对兔左室心肌细胞凋亡的影响。方法 采取末端脱氧核苷酸转移酶介导的dUTP -生物素平移末端标记 (TUNEL)技术和链酶亲和素 -生物素 -过氧化物酶复合物 (SABC)免疫组化方法 ,观察持续压力超负荷下兔左室心肌细胞凋亡的动态变化及bcl 2和bax蛋白的表达。结果 对照组出现极少量凋亡细胞 ,表达少量bcl 2蛋白 ,不表达bax蛋白。术后凋亡阳性心肌细胞数和bcl 2蛋白阳性表达心肌细胞数迅速增加 ,两者在心衰组最高。凋亡阳性心肌细胞数在术后第 3天多于术后第 7天。左室心肌细胞仅在术后第 1天组和心衰组表达bax蛋白。结论在持续压力超负荷所致心力衰竭的全过程 ,bcl 2蛋白都参与了抑制心肌细胞凋亡的调节 ,bax蛋白可能只参与了心肌细胞凋亡的启动。

Objective To study the effect of bcl 2 protein and bax protein expression on mytocyte apoptosis during chronic pressure overload in left ventricle of rabbit. Methods We investigated the dynamic changes of myocyte apoptosis and the expression of bcl-2 protein and bax protein in left ventricle of chronic pressure overload induced rabbit, using in situ terminal deoxynucleotidyl transferase mediated dUTP nick end labeling(TUNEL) and strept avidin biotin enzyme complex(SABC) immunohitochemistry. Results There were a few apoptosis and expression of bcl 2 protein in myocytes in control group. Normal myocyte of left ventricle did not express bax protein. The number of apoptosis and expression bcl-2 protein of myocyte in left ventricle were increased after operation,which were most remarkable in the group of congestive heart failure. Apoptosis in myocytes was more significant in 3 days after operation than that after 7 days.\ The expresion of bax protein was found only 1 day after operation and in the myocytes of congestive heart failure group.\ Conclusion During chronic pressure overload, bcl 2 protein may be participate in all the apoptotic process, and bax protein may be involved in the trigger mechanism of myocyte apoptosis.