丁酸钠对HepG2细胞诱导凋亡的作用及机制

目的探讨丁酸钠（sodium butyrate，SB）对HepG2细胞的诱导凋亡作用及与端粒酶活性的关系。方法采用MTT法检测5mmol／L丁酸钠在不同时间对HepG2细胞的增殖抑制作用；流式细胞仪检测丁酸钠作用于HepG2细胞后的凋亡情况，及细胞周期的改变；TRAP-ELISA法检测细胞端粒酶活性。结果丁酸钠能明显抑制HepG2细胞增殖，并且这种抑制作用具有时间依赖性。丁酸钠处理HepG2细胞48h凋亡率明显提高（P〈0．01），S期细胞比例显著下降（P〈0．05），G0／G1期细胞比例显著升高（P〈0．05）。实验组端粒酶活性为1.16±0．12，对照组端粒酶活性为3．58±0．33，实验组端粒酶活性明显降低（P〈0．05）。结论丁酸钠具有诱导HeoG2细胞凋亡的作用，其机制与抑制端粒酶活性有关。

Mechanism of Apoptosis in HepG2 Cell Line Induced by Sodium Buryrate

Objective To explore the effect of sodium butyrate on cell apoptosis of HepG2 cell line and its mechanism. Methods The proliferative activity of HepG2 cell line was observed by MTT assay. Flow cytometry was used to assess cell apoptosis after being treated by sodium butyrate. And TRAP-ELISA was applied to analyze telomerase activity of HepG2 cell. Results A time and dose dependent inhibition was remarkably confirmed in HepG2 cell line. As compared with control group, apoptosis rate of HepG2 cell line in research group increased obviously after being treated with sodium butyrate for 48 hours （P〈0.01 ）. The percentage of S phase decreased significantly（P〈0.05）, while the percentage of G0/G1 phase increased markedly（P〈0.05）. The activity of telomerase （ 1.16±0.12 ） in research group was significantly slower than that （3.58±0.33 ） in control group （P〈0.05）. Conclusion Sodium butyrate can greatly induce apoptosis of HepG2 cell line, and the inhibition oftelomerase activity plays an important role in the procedure ofapoptosis. There is a direct relationship between them.