【摘要】 目的 :探讨抗干血酸 (AA )对三氧化二砷(AT)诱导人肝癌细胞凋亡的协同效应 ,为改善三氧化二砷临床治疗人肝癌细胞提供理论基础。方法 :体外培养人肝癌细胞株BEL 74 0 2 ,用MTT和免疫印迹的方法分别评价AT和(或 )AA对其生长抑制和胞内两个信号分子的影响。结果 :微摩尔剂量的AT能抑制人肝癌细胞BEL 74 0 2的异常生长 ,通过caspase 3的激活诱导其凋亡 ,并激活了ERKs信号蛋白 ,其作用有明显的剂量依赖性。AA对BEL 74 0 2无明显的作用 ,但能有效的通过caspase 3而不是ERKs的激活促进AT对肝癌细胞的凋亡效应。结论 :ERKs和caspase 3信号蛋白可能分别参与了砷剂诱导的人肝癌细胞促分化和凋亡效应 ,AT和AA对肝癌细胞的作用有协同性 ,他们通过caaspase 3而不是ERKs的激活进一步抑制了肝癌的生长 ,诱导其凋亡。更多还原

【Abstract】 Objective: To study synergistic effect with Ascorbic acid(AA) on arsenic trioxide inducing human Hepatocarcinoma cell apoptosis, and provide theoretical basis for promoting human Hepatocarcinoma cell apoptosis induced by arsenic trioxide(AT). Methods: Human Hepatocarcinoma cell line BEL-7402 being cultured in vitro, the effect of AT and (or) AA on its growth inhibition and its two intracellular signal molecules was evaluated separately using MTT and Western blot. Results: AT at a few μmol/L concentration could suppress abnormal proliferation of human hepatocarcinoma cells, and initiate their apoptosis by activation of caspase-3, and activate extracellular-signal regulated kinases (ERKs), which were dependent on the dosage of AT conspicuously. The effect of AA on BEL-7402 was not significant; However, AA could effectively enhance AT-induced hepatocarcinoma cell apoptosis and lesion severity through activation of caspase-3 but not ERKs. Conclusion: Caspase-3 and ERKs proteins could involve in arsenic-induced hepatocarcinoma cell apoptosis and differentiation respectively as intracellular signaling molecules; The effect between AT and AA on hepatocarcinoma is synergistic, which further inhibits cell growth and induces apoptosis in human hepatocarcinoma cells through activation of caspase-3 but not ERKs.更多还原