黄芪甲苷对非小细胞肺癌A549细胞增殖及凋亡相关蛋白表达的影响

Effect of Astragaloside on proliferation and apoptosis-related protein expression of non-small cell lung cancer A549 cells

观察不同剂量的黄芪甲苷(As-Ⅳ)在体外对非小细胞肺癌(A549)细胞的生长、凋亡等方面的影响,探讨黄芪甲苷抑制A549细胞增殖、促进凋亡的可能分子机制。实验结果表明,As-Ⅳ作用24 h后,肺癌细胞A549的增殖明显受到抑制,具有剂量依赖性。A549细胞中的E-cadherin蛋白表达呈药物浓度依赖性上调,Vimentin蛋白表达下调。经As-Ⅳ作用24 h后的A549细胞,其胞质蛋白Bax/Bcl2表达水平高于对照组,同时As-Ⅳ也促使Caspase-3裂解为cleaved Caspase-3。黄芪甲苷在体外能抑制非小细胞肺癌A549细胞增殖、迁移并诱导其凋亡,其机制可能是通过抑制NEDD4/PTEN通路而激活并促进Bax表达的实现。该发现为临床上治疗非小细胞肺癌提供了有意义的实验依据。

Effects of different doses of astragaloside Ⅳ(As-Ⅳ) on the growth and apoptosis of non-small cell lung cancer A549 cells in vitro were observed, and the possible molecular mechanism of astragaloside Ⅳ in inhibiting the proliferation and promoting apoptosis of A549 cells was explored.The results showed that the proliferation of lung cancer cell A549 was significantly inhibited after the treatment of As-Ⅳ. Compared with the control group, the higher the concentration of drugs, the more obvious the inhibition rate of proliferation was in a dose-dependent manner. E-cadherin protein expression in A549 cells was up-regulated in a concentration-dependent manner, while Vimentin protein expression was down-regulated. The expression of Bax/Bcl2 in A549 cells treated with As-Ⅳ for 24 hours was higher than that in the control group. As-Ⅳ also promoted the Caspase-3 to cleaved Caspase-3. Astragaloside Ⅳ can inhibit proliferation, migration and induce apoptosis of non-small cell lung cancer A549 cells in vitro. Its mechanism may be to activate and promote the Bax expression by inhibiting NED4/PTEN pathway. This finding provides a meaningful experimental basis for the clinical treatment of non-small cell lung cancer.