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目的:探讨紫杉醇对体外培养的浆液性卵巢癌细胞HO-8910细胞凋亡的诱导作用。方法:体外培养卵巢癌细胞HO-8910,用浓度1×10-9 mol/L、1×10-8 mol/L、1×10-7 mol/L和1×10-6 mol/L的紫杉醇作用细胞12 h,24 h,48 h后,提取细胞DNA片段进行2.0 mg/L 琼脂糖凝胶电泳;消化HO-8910细胞并经碘化丙锭(IP)染色后,流式细胞仪(FCM)对细胞进行细胞周期分析;电子显微镜对紫杉醇作用后的HO-8910细胞进行形态学分析。结果:体外培养的卵巢癌HO-8910细胞经不同浓度的紫杉醇处理后,细胞生长明显受到抑制;于1×10-7 mol/L 紫杉醇作用48 h后可观察到细胞凋亡特异的DNA梯状电泳;流式细胞仪分析证实,细胞凋亡率达19.7 %;且电镜下可观察到典型的凋亡早期形态学改变。结论:卵巢癌HO-8910细胞对紫杉醇具有药物敏感性,紫杉醇对卵巢癌细胞的杀伤作用,是通过诱导细胞凋亡途径实现的。
Objective: To investigate the induction of paclitaxel on the apoptosis of ovarian cancer HO-8910 cells cultured in vitro. METHODS: HO-8910 ovarian cancer cells were cultured in vitro and treated with paclitaxel at concentrations of 1 × 10-9 mol / L, 1 × 10-8 mol / L, 1 × 10-7 mol / L and 1 × 10-6 mol / L Cells were treated with 2.0 mg / L agarose gel electrophoresis for 12 h, 24 h and 48 h. After digestion of HO-8910 cells with propidium iodide (IP), flow cytometry (FCM) ) Cell cycle analysis; electron microscopy of paclitaxel HO-8910 cells after morphological analysis. Results: The growth of ovarian cancer HO-8910 cells was inhibited by paclitaxel in different concentrations. The apoptosis-specific DNA ladder was observed after treated with paclitaxel (1 × 10-7 mol / L) for 48 h Electrophoresis; flow cytometry analysis confirmed that the rate of apoptosis was 19.7%; and electron microscopy can be observed under the morphological changes typical of early apoptosis. Conclusion: HO-8910 ovarian cancer cells have the drug sensitivity to paclitaxel, and the killing effect of paclitaxel on ovarian cancer cells is achieved through the induction of apoptosis pathway.