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目的研究冬凌草甲素(Oridonin,ORI)对膀胱癌T24细胞的作用及机制。方法MTT法检测ORI对T24细胞的生长抑制作用;光学显微镜和Hoechst 33258染色法荧光显微镜观察细胞的形态学变化;流式细胞仪检测凋亡变化;分光光度法检测Caspase 3的活性变化;Western blot检测bcl-2和bax表达的变化。结果ORI对T24细胞有明显的生长抑制作用,呈明显的时间-效应关系和浓度-效应关系。随着ORI作用时间延长,T24细胞凋亡增加,见凋亡小体出现。随着ORI作用时间的延长,T24细胞的Caspase 3活性逐渐增加,bcl-2的表达逐渐减弱,bax的表达逐渐增强。结论ORI对膀胱癌T24细胞有明显的诱导凋亡作用;机制可能是活化Caspase 3和下调bcl-2/bax。
Objective To investigate the effect and mechanism of Oridonin (ORI) on bladder cancer T24 cells. Methods MTT assay was used to detect the growth inhibition effect of ORI on T24 cells. Morphological changes of cells were observed by light microscopy and Hoechst 33258 staining, apoptosis was detected by flow cytometry, Caspase 3 activity was detected by spectrophotometry, Western blot Detection of bcl-2 and bax expression changes. Results ORI had obvious growth inhibitory effect on T24 cells, showing a significant time-effect relationship and concentration-effect relationship. With prolonged ORI effect, T24 cell apoptosis increased, see apoptotic bodies appear. With the prolongation of ORI, the activity of Caspase 3 in T24 cells gradually increased, the expression of bcl-2 gradually decreased and the expression of bax gradually increased. Conclusion ORI has obvious apoptosis-inducing effect on bladder cancer T24 cells. The mechanism may be activation of Caspase 3 and down-regulation of bcl-2 / bax.