短葶山麦冬皂苷C诱导人胃癌细胞SGC7901自噬机制初探 Molecular Mechanism of Liriope Muscari Baily Saponins C Induced Cellular Autophagy of SGC7901

以人胃癌细胞SGC7901为研究对象，探讨短葶山麦冬皂苷C的抗肿瘤作用及其分子机制。采用MTT检测、流式细胞仪分析、免疫蛋白印记实验，分别检测胃癌细胞SGC7901的增殖、凋亡及自噬。结果表明，短葶山麦冬皂苷C可抑制细胞增殖，但并不诱导细胞凋亡，可诱导细胞自噬，Western blotting检测结果表明短葶山麦冬皂苷C可引起自噬标志性蛋白Beclin-1表达增加及LC3-A转变为LC3-B。因此，短葶山麦冬皂苷C抑制胃癌细胞SGC7901增殖可能与凋亡无关，而是通过抑制经典的自噬信号转导通路Akt/mTOR诱导其发生自噬，从而发挥抗肿瘤作用。 This study is to investigate the antitumor activity of Liriope muscari baily saponins C. MTT, flow cytometric analysis and western blotting were to used to detect the proliferation activity, apoptosis and autophagy of SGC 7901. The results showed that Liriope muscari baily saponins C can inhibit cell proliferation, but it can induce autophagy, not apoptosis. Western blotting results showed that Liriope muscari baily saponins C can induce autophagy marker protein expression of Beclin-1 and make LC3-A become LC3-B. Therefore, this process is irrelevant to the apoptosis for inhibiting the proliferation of SGC7901, but it may induce autophagy by inhibiting the classical signal pathway of Akt/mTOR.