摘要
目的 :探讨PKC活化对大鼠I/R心肌细胞死亡和凋亡抑制基因bcl- 2表达的影响。方法 :采用TUNEL法以及免疫组化和原位杂交方法。结果 :①PMA +IR3h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IR3h组 (P <0 .0 5 ,<0 .0 1 ) ;②PMA +IR3h组表达Bcl- 2蛋白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多于IR3h组 (P <0 .0 1 ) ;PMA +IR1h组表达bcl- 2mRNA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多于IR1h组 (P <0 .0 1 )。结论 :①PKC活化能够显著减少大鼠I/R心肌细胞死亡 ;②PKC活化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。
AIM: To explore the effect of PKC activition on cardiac myocyte apoptosis and expression of bcl-2 during myocardial ischemia/reperfusion(I/R) in rats. METHODS: TUNEL,immunohistochemistry and in situ hybridization were used. RESULTS: The TUNEL data showed that the numbers of positive cardiac myocyte nucleus and the percentage of positive cardiac myocyte nucleus in PMA+IR 3 h group decreased significantly( P< 0.05, P< 0.01), compared to those in IR 3 h group. The number of Bcl-2 protein positive cardiomyocytes and the percentage of Bcl-2 protein positive cardiomyocytes in PMA+IR 3 h group were higher than those in IR 3 h group ( P< 0.01) bcl-2 mRNA expression showed the same changes in PMA+IR 0 h group compared to IR 1 h group. CONCLUSIONS: Activation of PKC decreased cardiomyocyte death during I/R. Upregulation of bcl-2 gene expression in cardiomyocytes during I/R may be one of the mechanisms of decreasing cardiomyocyte death by PCK activating during I/R.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第8期978-980,共3页
Chinese Journal of Pathophysiology