澳洲茄碱诱导胆管癌QBC939细胞凋亡及作用机制

Apoptosis-inducing Effects of Solasonine on Human Cholangiocarcinoma Epithelial QBC939 Cells and Its Mechanism

研究澳洲茄碱对人胆管癌上皮细胞系QBC939凋亡的诱导与作用机制。采用MTT法检测不同浓度澳洲茄碱对QBC939细胞的增殖抑制作用;流式细胞术检测澳洲茄碱对QBC939细胞的凋亡诱导情况;Western blot检测澳洲茄碱对QBC939细胞中凋亡相关蛋白(Bax、Bcl-2、caspase3、caspase7、PARP、cleaved PARP)的表达影响。结果发现澳洲茄碱以浓度依赖方式能够抑制QBC939细胞的增殖;澳洲茄碱能够显著诱导QBC939细胞的凋亡;澳洲茄碱可以上调Bax、caspase3、caspase7和cleaved PARP蛋白表达,下调Bcl-2和PARP蛋白表达。表明澳洲茄碱能够通过改变凋亡相关蛋白表达,诱导胆管癌QBC939细胞的凋亡,这对于研发和治疗胆管癌相关药物具有一定的潜在价值。

This study focused on investigating the effect of solasonine on human cholangiocarcinoma epithelial QBC939 cells via inducing apoptosis and related mechanisms. MTF assay was used to detect the inhibition effect of solasonine on QBC939 cell proliferation, flow cytometry was applied to detect QBC939 cells apoptosis induced by solasonine, Western blot was used to detect the expression changes of apoptosis-related proteins （ Bax, Bcl-2, caspase3, caspase7, XIAP, PARP, cleaved PARP） induced by solasonine in QBC939 cells. The results showed that solasonine can inhibit the prolif- eration of QBC939 cells in a dose-dependent manner significantly, solasonine can induce apoptosis of QBC939 cells obvi- ously, and solasonine can increase protein expression level of Bax, caspase3, caspase7 and cleaved PARP and decrease the protein expression level of Bcl-2, XIAP and PARP. Those results suggested that solasonine can induce apoptosis of cholangiocarcinoma QBC939 cells significantly by changing the expression of apoptosis-related protein, which had the po- tential to be the drug candidate for the treatment of human cholangiocarcinoma in future.