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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。
Objective: To investigate the synergistic effect of anti-dry acid (AA) on apoptosis in human hepatoma cells induced by arsenic trioxide (AT) and to provide a theoretical basis for the clinical treatment of human hepatoma cells with arsenic trioxide. Methods: Human hepatocellular carcinoma cell line BEL-7402 was cultured in vitro. The effects of AT and / or AA on the growth inhibition and intracellular signaling molecules were evaluated by MTT and Western blot respectively. Results: A dose of AT could inhibit the abnormal growth of human hepatocellular carcinoma cell line BEL-7402, induce its apoptosis through the activation of caspase 3 and activate the ERKs signaling protein in a dose-dependent manner. AA has no obvious effect on BEL 74 0 2, but it can effectively promote the apoptosis effect of AT on liver cancer cells through the activation of caspase 3 instead of ERKs. CONCLUSIONS: ERKs and caspase 3 signaling proteins may be involved in the arsenic-induced human hepatocellular carcinoma cell differentiation and apoptosis, respectively. AT and AA have synergistic effects on hepatocarcinoma cells. They further inhibit the activation of caaspase 3 but not ERKs Liver cancer growth, induction of apoptosis.