论文部分内容阅读
目的 :探讨阿霉素诱导卵巢癌细胞凋亡的规律。方法 :以不同浓度的阿霉素作用于人卵巢癌细胞株SKOV3,用光镜、电镜、TUNEL法和DNA凝胶电泳法检测确定细胞凋亡 ,以流式细胞仪定量分析凋亡和细胞周期特异性。结果 :大剂量 ( 2 5～10 0 μg/ml)长时间 ( 3～ 72h)的阿霉素作用可引起卵巢癌细胞坏死和凋亡 ,较小剂量( 0 .5μg/ml)的阿霉素连续作用 2 4、4 8、72h ,诱导细胞凋亡发生率分别为 4 0 .0 1%、65.38%和 77.65% ,并使细胞发生G1期阻滞。结论 :阿霉素能导致卵巢癌细胞DNA损伤 ,发生G1期阻滞并诱导凋亡是其抗肿瘤的机制之一。
Objective: To investigate the regulation of apoptosis induced by adriamycin in ovarian cancer cells. METHODS: Human ovarian cancer cell line SKOV3 was treated with different concentrations of doxorubicin. Cell apoptosis was determined by light microscopy, electron microscopy, TUNEL method and DNA gel electrophoresis. Apoptosis and cell cycle were analyzed by flow cytometry. Specificity. RESULTS: Large doses (25 to 100 μg/ml) of doxorubicin for a long time (3 to 72 hours) could cause necrosis and apoptosis of ovarian cancer cells. Small doses (0.5 μg/ml) of doxorubicin After continuous exposure for 24, 48, and 72h, the induction rate of apoptosis was 40.0%, 65.38%, and 77.65%, respectively, and G1 arrest of cells occurred. Conclusion: Doxorubicin can induce DNA damage in ovarian cancer cells. G1 arrest and induction of apoptosis are one of the mechanisms of its anti-tumor effect.