预处理对缺血再灌注心肌细胞即刻早期基因c-fos、c-jun表达的调控

REGULATION OF PRECONDITIONING ON EXPRESSION OF PROTO-ONCOGENES c-fos, c-jun IN ISCHEMIA-REPERFUSION CARDIOMYOCYTES

为探讨即刻早期基因在预处理中的作用机制 ,将培养心肌细胞分别经短暂缺血及佛波酯、去甲肾上腺素、腺苷预处理 ,行模拟缺血再灌注 ,采用Northern杂交技术对心肌细胞c fos、c junmRNA含量进行检测。结果发现 ,缺血预处理组c fos、c junmRNA明显上升 ,其他药物预处理组c fos、c jun基因均有不同程度的表达增强 ,H7能明显抑制预处理对c fos、c junmRNA的诱导。表明预处理可能通过激活PKC ,进而诱导c fos、c jun基因的转录表达增强 。

To probe into the mechanism of c fos, c jun expression regulated by preconditioning, we observed protein kinase C (PKC) changes of c fos, c jun gene transcription in cultured cardiomyocytes affected by transient ischemic and medicine preconditioning mimicking ischemia reperfusion injury. Cultured rat cardiac myocytes were exposed to ischemia reperfusion mimicking solution after brief ischemic episodes or PMA, norepinephrine, adenosine preconditioning. Using Northern hybridization assay, we detected the gene transcription of c fos, c jun in cardiomyocytes. In mimicking ischemia the content of c fos, c jun mRNA increased significantly. Drug preconditioning induced cardiomyocyte c fos ,c jun expression in varing degrees. H 7 blocked this preconditioning effect. These results suggest that through activating PKC preconditioning induced c fos, c jun expression and PKC might play a central role in ischemic preconditioning.