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目的:研究雷公藤甲素对正常人肝细胞株L-02细胞凋亡诱导的作用及对细胞内钙离子及p38MAPK磷酸化的影响。方法:体外培养L-02细胞,Fluo-3AM标记与PI法观察雷公藤甲素对细胞的损伤作用,并测定雷公藤甲素作用下L-02细胞内钙离子浓度及Phospho-p38与Total-p38的含量。结果:雷公藤甲素体外诱导L-02细胞损伤,随着孵育时间的延长,细胞内钙离子浓度升高,至9h时达峰值(P<0.01),12h时有所下降(P<0.05);同时,雷公藤甲素促进细胞中P38MAPK的磷酸化(P<0.01),但对Total-p38无影响。结论:细胞内钙离子的释放及p38MAPK的磷酸化可能参与了雷公藤甲素引起的L-02细胞毒性。
Objective: To study the effect of Triptolide on apoptosis induction of normal human hepatocyte cell line L-02 and its effect on phosphorylation of intracellular calcium and p38MAPK. Methods: L-02 cells were cultured in vitro. Fluo-3AM and PI were used to observe the effect of triptolide on cell injury. The intracellular Ca2 + concentration and phosphorylation of Phospho-p38 and Total- p38 content. Results: Triptolide induced L-02 cell injury in vitro. With the extension of incubation time, intracellular calcium concentration increased, reaching the peak value at 9h (P <0.01) and decreased at 12h (P <0.05) At the same time, triptolide promoted the phosphorylation of P38MAPK in cells (P <0.01), but had no effect on Total-p38. Conclusion: The release of intracellular Ca2 + and the phosphorylation of p38MAPK may be involved in triptolide-induced cytotoxicity of L-02.