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目的:探讨冬凌草甲素抑制人雄激素非依赖性前列腺癌细胞株PC-3细胞的增殖、诱导其凋亡的作用。方法:用不同浓度的冬凌草甲素干预PC-3细胞,通过MTT实验和细胞的药物浓度-时间生长曲线分析观察其对PC-3细胞活力的影响;用流式细胞仪分析PC-3早期凋亡细胞的百分率;Western印迹检测BaxBcl-2和caspase-3蛋白表达的变化。结果:冬凌草甲素呈时间和浓度依赖性地抑制PC-3细胞增殖,药物抑制PC-3细胞活力的IC50约为10.29μmol/L;凋亡细胞形态学鉴定、流式细胞仪检测结果均表明冬凌草甲素能以浓度依赖性方式诱导PC-3细胞凋亡(P<0.05);冬凌草甲素以浓度依赖性方式抑制PC-3细胞的Bcl-2蛋白表达,而上调Bax蛋白表达并活化caspase-3。结论:冬凌草甲素可能通过线粒体途径诱导PC-3细胞凋亡。
Objective: To investigate the effect of oridonin on the proliferation and induction of apoptosis in human androgen-independent prostate cancer cell line PC-3. Methods: PC-3 cells were treated with different concentrations of oridonin. The effects of oridonin on the viability of PC-3 cells were observed by MTT assay and drug concentration-time curve. The expression of PC-3 The percentage of apoptotic cells was detected by Western blotting. The protein expression of BaxBcl-2 and caspase-3 were detected by Western blotting. Results: Oridonin inhibited the proliferation of PC-3 cells in a concentration-dependent and time-dependent manner. The IC50 of the drug for inhibiting the viability of PC-3 cells was about 10.29μmol / L. The morphological characteristics of apoptotic cells and the results of flow cytometry All showed that oridonin could induce apoptosis of PC-3 cells in a concentration-dependent manner (P <0.05). Oridonin inhibited the expression of Bcl-2 protein in PC-3 cells in a concentration-dependent manner, Bax protein expression and activation of caspase-3. Conclusion: Rubescensine A may induce PC-3 cell apoptosis through mitochondrial pathway.