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目的探讨米非司酮在体外诱导雄激素非依赖性前列腺癌DU-145、PC-3细胞凋亡的作用。方法采用四甲基偶氮唑蓝法检测1,10,50和100μmol/L米非司酮作用于前列腺癌DU-145、PC-3细胞24~120h的吸光度(A)值,用流式细胞仪检测10μmol/L米非司酮作用24和48h后DU-145、PC-3细胞凋亡率的变化;采用免疫组化法检测米非司酮作用DU-145、PC-3细胞后bax、bcl-2、血管内皮生长因子(VEGF)蛋白表达的变化。结果1μmol/L米非司酮组的A值与对照组相比,差异无统计学意义(P>0.05);10,50和100μmol/L米非司酮组的A值与对照组比较,差异有统计学意义(P<0.01);米非司酮对前列腺癌DU-145、PC-3细胞的抑制作用呈时间-剂量依赖性。10μmol/L米非司酮作用前列腺癌DU-145细胞24和48h的凋亡率分别为15.3%和30.4%,PC-3细胞的凋亡率分别为22.2%和32.0%。经10μmol/L米非司酮作用后,DU-145、PC-3细胞中VEGF和bcl-2蛋白的表达明显减少,而bax的表达显著增加(P<0.05)。结论米非司酮以时间-剂量依赖性方式抑制激素非依赖性前列腺癌DU-145和PC-3细胞的增殖,其作用可能是通过降低VEGF蛋白的表达,从而下调bcl-2、激活bax蛋白的表达来实现。
Objective To investigate the effect of mifepristone on the apoptosis of androgen-independent prostate cancer DU-145 and PC-3 cells in vitro. Methods Absorbance (A) values of 1, 10, 50 and 100 μmol / L mifepristone on prostate cancer DU-145 and PC-3 cells were detected by MTT method. The changes of apoptosis rate of DU-145 and PC-3 cells after treatment with 10 μmol / L mifepristone for 24 and 48 h were detected by immunohistochemistry. The expression of bax, bcl-2, vascular endothelial growth factor (VEGF) protein expression changes. Results There was no significant difference in the A value between the mifepristone group and the control group (P> 0.05). The A value of the mifepristone group at 10, 50 and 100μmol / L was significantly lower than that of the control group (P <0.01). The inhibitory effect of mifepristone on DU-145 and PC-3 cells in a time and dose-dependent manner. The apoptotic rates of DU-145 cells treated with 10μmol / L mifepristone were 15.3% and 30.4% at 24 and 48h, respectively. The apoptosis rates of PC-3 cells were 22.2% and 32.0%, respectively. After treated with 10μmol / L mifepristone, the expression of VEGF and bcl-2 protein in DU-145 and PC-3 cells was significantly decreased, while the expression of bax was significantly increased (P <0.05). Conclusions Mifepristone inhibits the proliferation of hormone-independent prostate cancer DU-145 and PC-3 cells in a time-and-dose-dependent manner by down-regulating bcl-2 and activating bax protein by decreasing the expression of VEGF protein To achieve the expression.