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本实验用无血清的培养新生大鼠心肌细胞，探讨内皮素１（ＥＴ１）对原癌基因ｃｆｏｓ表达的作用。结果显示：ＥＴ１可显著诱导ｃｆｏｓ的表达，其表达的高峰在３０ｍｉｎ，２ｈ恢复到正常水平，并呈剂量依赖性反应和被ＥＴＡ的特异性受体拮抗剂ＢＱ１２３所阻断；蛋白激酶Ｃ（ＰＫＣ）激动剂ＰＭＡ可诱导ｃｆｏｓ表达，而ＰＫＣ抑制剂Ｓｔａｕｒｏｓｐｏｒｉｎｅ则可阻断ＥＴ１诱导的ｃｆｏｓ表达；钙通道阻断剂硝苯吡啶预处理心肌细胞对ＥＴ１诱导的心肌细胞的ｃｆｏｓ表达无明显的作用。这些结果提示，ＥＴ１诱导ｃｆｏｓ表达是通过ＥＴＡ受体介导的，ＰＫＣ在此过程中起重要作用。
In this study, serum-free cultured cardiomyocytes of neonatal rats to explore the role of endothelin 1 (ET 1) proto-oncogene cfos expression. The results showed that: ET 1 can significantly induce the c fos expression, the peak of expression at 30min, 2h returned to normal levels, and a dose-dependent response and ETA-specific antagonist BQ123 block; protein PKC agonist PMA can induce c fos expression, and PKC inhibitor Staurosporine can be blocked ET 1 induced c fos expression; calcium channel blocker nifedipine pretreatment of myocardial cells ET 1 Induced cardiomyocyte c fos expression had no significant effect. These results suggest that ET 1-induced c-fos expression is mediated through the ETA receptor, PKC plays an important role in this process.