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目的 探讨二十碳五烯酸 (eicosapentaenoicacid ,EPA)对 3种肝癌细胞系作用。方法EPA作用于HepG2 (携带有野生型p5 3基因 )、Huh7(携带有突变型p5 3基因 )和Hep3B(p5 3基因缺失 )这 3种肝癌细胞系 ,通过细胞计数、DNA电泳、流式细胞技术和末端转移酶标记技术等来检测EPA对这 3种细胞系的作用和可能的机制。结果 EPA主要是通过诱导HepG2肝癌细胞系的细胞凋亡来抑制其生长 ,而且这种抑制作用呈现出时间和剂量依赖的关系 ,而且同时发现EPA对于Huh7和Hep3B这两种肝癌细胞系无明显抑制作用。结论 细胞凋亡的诱导可能是EPA抑制HepG2肝癌细胞系生长的主要机制 ,而且p5 3基因可能参与EPA诱导HepG2细胞系细胞凋亡的过程。
Objective To investigate the effects of eicosapentaenoic acid (EPA) on three hepatoma cell lines. Methods EPA was applied to HepG2 (carrying wild-type p53 gene), Huh7 (carrying mutant p53 gene) and Hep3B (p53 gene deletion), three hepatocellular carcinoma cell lines, by cell counting, DNA electrophoresis, flow cytometry Techniques and terminal transferase labeling techniques were used to examine the effects and possible mechanisms of EPA on these three cell lines. RESULTS EPA inhibited the growth of HepG2 hepatocarcinoma cells by inducing apoptosis, and this inhibition exhibited a time- and dose-dependent relationship. At the same time, it was found that EPA did not significantly inhibit the two hepatoma cell lines Huh7 and Hep3B. effect. Conclusion The induction of apoptosis may be the main mechanism of EPA inhibiting the growth of HepG2 hepatocellular carcinoma cell line, and p53 gene may be involved in the process of apoptosis induced by EPA in HepG2 cell line.