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目的:探讨常春藤皂苷元对前列腺癌细胞增殖、迁移和侵袭能力的影响,以及可能的机制。方法:培养人前列腺癌细胞株DU145,分别加入不同浓度常春藤皂苷元(25、50、100μg/ml)作用于DU145细胞,继续培养12、24、36、48h,采用MTT法检测不同浓度常春藤皂苷元对DU145细胞增殖的影响;流式细胞术检测细胞凋亡;利用Transwell小室检测细胞迁移和侵袭能力;利用实时荧光定量PCR检测Bcl-2、Bax、PI3K、Akt基因表达,利用Western blot检测Bcl-2、Bax、PI3K、p-PI3K、Akt和p-Akt蛋白表达。结果:随着常春藤皂苷元浓度(25、50、100μg/ml)的增加,可显著抑制DU145细胞的增殖,这种抑制作用具有时间和剂量依赖性;随着常春藤皂苷元浓度(25、50、100μg/ml)的增加,DU145细胞细胞凋亡率升高;与对照组相比,常春藤皂苷元能显著抑制DU145细胞迁移和侵袭能力;常春藤皂苷元不同浓度组处理DU145细胞48h后,随着常春藤皂苷元浓度升高,Bcl-2、PI3K、Akt mRNA和蛋白相对表达量下降,而Bax mRNA和蛋白相对表达量升高。结论:常春藤皂苷元可抑制前列腺癌细胞增殖、迁移及侵袭能力,促进细胞凋亡发生,且表现出一定的剂量-反应关系,其机制可能与抑制PI3K/Akt信号通路有关。
Objective: To investigate the effect of ivy saponin on the proliferation, migration and invasion of prostate cancer cells and the possible mechanism. Methods: Human prostate cancer cell line DU145 was cultured and treated with different concentrations of ivygenin (25, 50, 100μg / ml) for DU145 cells. The cells were cultured for 12, 24, 36 and 48 hours. The effect of sapogenin on the proliferation of DU145 cells was detected by flow cytometry. The apoptosis of DU145 cells was detected by flow cytometry. The ability of cell migration and invasion was detected by Transwell chamber. The expression of Bcl-2, Bax, PI3K and Akt was detected by real-time fluorescence quantitative PCR. Bcl-2, Bax, PI3K, p-PI3K, Akt and p-Akt protein expression. Results: The proliferation of DU145 cells was significantly inhibited with the increase of the concentration of hepatigenin (25, 50, 100μg / ml). The inhibitory effect was dose-dependent and time-dependent. With the increase of the concentration of hematogen saponins (25, 50,100μg / ml) increased the apoptosis rate of DU145 cells; compared with the control group, ivy saponins significantly inhibited DU145 cell migration and invasion ability; ivy saponin different concentrations of group treated DU145 cells 48h , The relative expression of Bcl-2, PI3K, Akt mRNA and protein decreased while the expression of Bax mRNA and protein increased with the increase of the concentration of Ivy saponin. Conclusion: Ivy sapogenin can inhibit the proliferation, migration and invasion of prostate cancer cells and promote the apoptosis of cells, and show a dose-response relationship. The mechanism may be related to the inhibition of PI3K / Akt signaling pathway.