澳洲茄碱抑制人膀胱癌5637细胞增殖及其机制研究

Inhibition of proliferation on human bladder cancer cell 5637 by solasonine and its mechanisms

[目的]探究澳洲茄碱对人膀胱癌细胞株5637细胞增殖的影响,并初步揭示其相关机制,为膀胱癌治疗提供新的方向。[方法]以人膀胱癌5637细胞为研究对象,将浓度为5、10、20、40、80μmol/L的澳洲茄碱分别作用于细胞24h、48 h、72 h,MTT法计算各组细胞增殖率,据此设置空白对照组、溶剂对照组、以及不同浓度梯度(10、20、40、80μmol/L)的澳洲茄碱处理组作为后续实验分组。24 h后使用显微镜观察细胞形态变化,Western Blotting检测相关凋亡蛋白Bax、Bcl-2、Caspase-3的表达变化情况。[结果]10μmol/L的澳洲茄碱在24 h时即可显著地抑制5637细胞的增殖,且抑制作用具有时间和浓度依赖性;澳洲茄碱处理后的5637细胞具有细胞凋亡形态学变化;Western Blotting结果表明,在一定浓度范围内,与空白对照组相比,促凋亡蛋白Bax、Caspase-3表达量随澳洲茄碱浓度增大而升高,而抑凋亡蛋白Bcl-2表达量下降,差异均具有统计学意义(P<0.05)。[结论]澳洲茄碱可抑制人膀胱癌5637细胞增殖,其机制之一是通过调控凋亡相关蛋白Bax、Bcl-2及Caspase-3的表达而诱导细胞凋亡。

[Objective]To investigate the effect of solasonine on proliferation in human bladder cancer cell line 5637,and reveal its relevant mechanisms.Providing a new direction for the treatment of bladder cancer.[Method]Human bladder cancer5637 cells were taken as research objects and treated with solasonine at different concentrations(0,10,20,40,80μmol/L)for24 hours,48 hours and 72 hours respectively.The rate of cell proliferation was calculated by MTT assay.Accordingly,the blank control group,the solvent control group,and solasonine treatment group with different concentration gradients(10,20,40,80μmol/L)were set as follow-up groups.After 24 hours,the cell morphology changes were observed under an inverted optical microscope;And the expression changes of apoptosis-related proteins Bax,Bcl-2 and Caspase-3 were detected by Western Blotting.[Result]Solasonine significantly inhibited the proliferation of 5637 cells at 10μmol/L,24 hours,and the inhibition was time-and concentration-dependent.After treated with solasonine,cells showed morphology apoptotic changes.Western Blotting results showed that within a certain range,the expression of Bax and Caspase-3 increased,while Bcl-2 decreased with increased solasonine concentration,and both the differences were statistically significant(P<0.05).[Conclusion]Solasonine can inhibit the proliferation of human bladder cancer 5637 cells,and one of the mechanisms was inducing the apoptosis of5637 cells by regulating the expression of apoptosis-related proteins Bax,Bcl-2 and Caspase-3.