中文摘要：

目的探讨蛋白激酶C（PKC）活性改变对HSC表达TGF β1的影响及在HSC激活中的作用。方法将肝星状细胞系rHSC-99分为3组：对照组（A组），PKC激动剂佛波酯0．5μmol／L组（B组），PKC抑制剂Calphostin C 100nmol／L组（C组）。加药后0、3、6、12h和24h分别检测各组细胞PKC活性的变化；作用24h后，采用Western blot和RT—PCR方法检测各组细胞TGF β1，Smad 4，Ⅰ、Ⅲ型胶原和α-平滑肌肌动蛋白的表达；采用MTT法检测细胞的增殖情况。结果 佛波酯作用后PKC的活性显著增强，而Calphostin C则抑制PKC的活性。PKC活性增强后，与对照组相比TGF β1及其下游信号分子Smad 4的表达分别升高了4．8倍和13．1倍（P〈0．01）；HSC的Ⅰ、Ⅲ型胶原和α-平滑肌肌动蛋白的表达分别升高了2．4倍、1．8倍和1．3倍（P〈0．01），并促进HSC的增殖；PKC活性被抑制后则能抑制以上作用。结论PKC活性的改变能调控HSC中TGF β1的表达，在HSC的激活中发挥调节作用。

英文摘要：

Objective To investigate the effect of protein kinase C （PKC）/transforming growth factor beta 1 （TGFβ1） pathway on activation of hepatic stellate cells （HSC）. Methods HSC rHSC-99 cell line was used in three groups in this study. Group A served as a control. In group B the HSC were incubated with PKC agonist PMA （0.5 μmol/L）, and in group C the cells were incubated with PKC inhibitor calphosfin C （ 100 nmol/L）. The PKC activities were detected at different incubation time points （0, 3, 6, 12 and 24 h）. Western blot and RTPCR were used to detect the expression of TGF β1, Smad 4, collagen type Ⅰ, Ⅲ and α-smooth muscle actin （ α -SMA） at the 24 h point. Cell proliferation was assessed by MTT colorimetric assay. Results PMA increased the activity of PKC significantly, whereas calphostin C inhibited the activity of PKC. The increased activity of PKC promoted the HSC to express TGF β1, Smad 4, collagen type Ⅰ, Ⅲ and α -SMA. In comparison with the controls, the expressions of TGF β1, Smad 4, collagen type Ⅰ, Ⅲ and α -SMA increased 4.8, 13.1, 2.4, 1.8 and 1.3 fold respectively （P 〈 0.01）. PKC promoted the proliferation of HSC. The above effects were inhibited by the inhibition of PKC activity. Conclusion Changing of PKC activity can regulate and control the expression of TGF β1, which may play a role in regulating the activation of HSC.