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探讨蛋白激酶C（PKC）信号通道对体外培养的正常成年牛肺动脉平滑肌细胞（PA SMC）增生的调控作用。结果:PKC活化剂PMA（phorbol 12-myristate 13-acetate）可明显刺激PA SMC增生,PMA为10nmol/L时,3~H胸腺嘧啶掺入率由对照组的（44.9±10.6）min~（-1） /孔增加到（5904.7±607.6）min~（-1）/孔,p<0.01;预先应用PKC抑制剂可阻断PMA的刺激作用,3~H胸腺嘧啶掺入率由（5 117.1±756.2）min~(-1)/孔减少至（90.2±5.3）min~(-1)/孔;3种不同的PKC抑制方法均可部分阻断100ml/L小牛血清对PA SMC增生的刺激作用（均为 P<0.01）;在 PA SMC的全细胞溶解产物中可直接测到PKC酶活性,而经钝化处理后该酶活性消失（P<0.01 ）,与钝化处理可部分阻断血清的PA SMC增生刺激作用相吻合。提示PKC信号通道是PA SMC增生的调控机制之一。
To investigate the regulatory effect of protein kinase C (PKC) signaling pathway on hyperplasia of normal adult bovine pulmonary artery smooth muscle cells (PA SMC) cultured in vitro. Results: Phospholipase 3 (3) H thymidine incorporation was significantly increased from (44.9 ± 10.6) min to (-) in the control group at a PMA of 10 nmol / 1) / well increased to (5904.7 ± 607.6) min ~ (-1) / well, p <0.01. Pretreatment with PKC inhibitor blocked the stimulation of PMA, and the incorporation rate of 3 ~ H thymidine was (5 117.1 ± 756.2) min / (-1) / well decreased to (90.2 ± 5.3) min ~ (-1) / well. Three different PKC inhibition methods could partly block the stimulation of proliferation of PA SMCs by 100 ml / L bovine serum (All P <0.01). The activity of PKC could be detected directly in whole cell lysates of PA SMC, but disappeared after passivation (P <0.01), and partially blocked by passivation Serum PA SMC hyperplasia stimulation consistent. Suggesting that PKC signaling pathway is one of the regulatory mechanisms of PA SMC proliferation.