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目的观察雌马酚(equol)对人卵巢癌SKOV-3细胞增殖的抑制作用,并探讨其作用的分子机制。方法用不同浓度(10-8、10-7、10-6、10-5、5×10-5、10-4mol/L)雌马酚处理SKOV-3细胞24、48、72h后,及同时用10μmol/LERK通路抑制剂U0126或雌激素受体抑制剂ICI182,780处理1h后再用50μmol/L雌马酚处理2h,测定各组SKOV-3细胞存活率,用Westernblotting检测总ERK和磷酸化ERK1/2(p-ERK)的蛋白表达水平。结果各实验组SKOV-3细胞存活率随着雌马酚作用浓度和时间的增加而降低,总ERK蛋白表达量不变,p-ERK的表达量随雌马酚处理浓度的增加而逐渐降低。U0126、ICI182,780单独使用或与雌马酚联合使用均能够降低p-ERK的蛋白表达。结论雌马酚显著抑制人卵巢癌SKOV-3细胞的增殖,其机制是通过下调磷酸化ERK蛋白的表达发挥作用。
Objective To observe the inhibitory effect of equol on the proliferation of human ovarian cancer SKOV-3 cells and to explore its molecular mechanism. Methods SKOV-3 cells were treated with different concentrations (10-8, 10-7, 10-6, 10-5, 5x10-5 and 10-4 mol / L) of equol for 24, 48 and 72 hours, After treated with 10μmol / L ERK inhibitor U0126 or estrogen receptor inhibitor ICI182,780 for 1h and then treated with 50μmol / L equol for 2h, the survival rate of SKOV-3 cells in each group was determined. The total ERK and phosphorylation ERK1 / 2 (p-ERK) protein expression levels. Results The survival rate of SKOV-3 cells in each experimental group decreased with the increase of concentration and time of equol, while the expression of total ERK protein remained unchanged. The expression of p-ERK decreased gradually with the increase of equol concentration. U0126, ICI182,780, alone or in combination with equol, were able to reduce p-ERK protein expression. Conclusion Equol can significantly inhibit the proliferation of human ovarian cancer SKOV-3 cells by down-regulating the expression of phosphorylated ERK protein.