丝裂原活化蛋白激酶在大黄素收缩大鼠胃平滑肌细胞中的作用

[目的]研究丝裂原活化蛋白激酶(MAPK)在大黄素对大鼠胃平滑肌细胞收缩信号转导途径中的作用机制。[方法]酶解法分离的大鼠胃平滑肌细胞经过培养后分为3个实验组:空白对照组、大黄素组、蛋白激酶C(PKC)抑制剂组(Calphostin C 大黄素)。通过Western blotring方法分析p44／42 MAPK在不同实验组中的表达量变化。[结果]磷酸化p44／42 MAPK的表达量在对照组最少,大黄素组最多,抑制剂组表达量较大黄素组少;三组表达量的差别具有显著性(P值均<0．01)。[结论]磷酸化p44／42 MAPK的表达量变化说明,在相同实验条件下,PKC受抑制后,磷酸化p44／42 MAPK的表达明显低于未受抑制的试验组。本实验结果提示, PKC到p44／42 MAPK信号转导通路参与了大黄素对大鼠胃平滑肌细胞收缩活动的调节。

Mechanism of MAPK in contractile effects of Emodin on the smooth muscle cells of rat stomach

[Objective] To investigate the role of MAPK in the signal transduction pathway of the contractile effects induced by Emodin in smooth muscle cells of rat stomach. [Methods] Smooth muscle cells of rat stomach were isolated and cultured. The cells were divided into 3 groups randomly: blank control group, Emodin group, inhibitor group. In Emodin group, the cells were treated by Emodin (50 mM, 1 min) . In inhibitor group, the cells were treated by Calphostin C for 60 mins, then treated by Emodin (50 mM, 1 min) . Phospho-p44/42 MAPK expression changes in the three groups were detected by Western blotting. [Results] Western blotting showed that the expression of phospho-p44/42 MAPK in the three groups was significant difference. [Conclusion] Calphostin C inhibited the activition of PKC and caused the decrease of the expression of phospho-p44/42 MAPK. The signal transduction way of PKC to phospho-p44/42 MAPK takes part in the contracting regulation of smooth muscle cell reduced by emodin.