2-甲氧基雌二醇诱导卵巢癌细胞凋亡的研究

目的探讨2-甲氧基雌二醇（2-ME）诱导卵巢癌细胞系OVCAR-3细胞和卵巢癌原代培养细胞凋亡的作用及其机制。方法以2-ME作用于卵巢癌OVCAR-3细胞和原代培养细胞，采用MTT法检测细胞存活率、Annexin V—FITC／PI双染流式细胞术检测细胞凋亡，JC-1染色流式细胞术检测细胞线粒体膜电位（△ψm），比色测定试剂盒检测caspase-3和caspase-8活性。结果与对照组相比，OVCAR-3细胞2-ME组存活率显著下降（100％vs70．5％），凋亡率明显增加（5．3％VS40．5％）；卵巢癌原代培养细胞2-ME组存活率显著下降（100％vs61．8％），凋亡率明显增加（5．4％VS36．9％）；此外，2-ME明显降低卵巢癌OVCAR-3细胞和原代培养细胞的AtOm，提高caspase-3和caspase-8活性。而预先以Z—VAD阻断caspase能逆转2-ME的效应。结论2-ME通过凋亡信号通路的内源性和外源性途径，诱导卵巢癌细胞凋亡。

Study of 2-methoxyestrodial inducing apoptosis in ovarian cancer cells

Objective To investigate the effects of 2-methoxyestrodial (2-ME)on the apoptosis of human ovarian cancer cells and explore its mechanisms.Methods Human ovarian cancer cell line OVCAR-3 cells and primary cultured cells were treated with 2-ME.Cell viability was examined by MTT as-say.Apoptosis was determined Annexin V-FITC/PI staining and flow cytometry.Mitochondrial membrane potential(△Ψm)was analyzed by JC-1 staining and flow cytometry.Caspase-3 and caspase-8 activity was measured by colorimetric assay kits.Results 2-ME inhibited viability in OVCAR-3 cells(100%vs70.5%)and primary cultured cells(100%vs 61.8%),increased apoptosis in OVCAR-3 cells(5.3%vs 40.5%)and primary cultured cells(5.4%vs 36.9%),decreased △Ψm and increased caspase-3 and caspase-8 activity in ovarian cancer cell line OVCAR-3 cells and primary cultured cells.In addition,its effects could be reversed by pan-caspase inhibitor Z-VAD.Conclusion 2-ME can induce apoptasis in hu-man ovarian cancer cells by activation of both intrinsic and extrinsic apoptotic pathways.