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机构地区:[1]复旦大学妇产科医院,上海200032 [2]复旦大学上海医学院生化系
出 处:《现代妇产科进展》2003年第2期93-95,F003,共4页Progress in Obstetrics and Gynecology
摘 要:目的:探讨三氧化二砷对体外培养的SKOV3细胞的生物学效应和作用机制。方法:用MTT法、流式细胞术、电镜检测体外培养的SKOV3细胞在三氧化二砷作用下的增殖抑制及凋亡程度,用RT-PCR法检测P53/Bcl-2/Bax的mRNA水平。结果:(1)三氧化二砷对SKOV3细胞的增殖抑制作用随浓度升高和作用时间延长而明显增强,其72hIC50约6μmol/L;(2)流式细胞术证实6μmol/L三氧化二砷作用24h能使SKOV3出现G2M阻滞,作用72h诱导细胞凋亡达高峰,凋亡率为18.60%,作用96h则趋向坏死;6μmol/L三氧化二砷作用72h用电镜术也检测到凋亡细胞存在。(3)RT-PCR法显示SKOV3细胞在6μmol/L三氧化二砷作用2h、6h、24h、48h均显示Bax上调和Bcl-2的下调,其中Bax的上调以2h最显著。而Bcl-2的表达则随作用时间延长而逐渐下降,P53则未检测到表达。结论:在体外三氧化二砷能抑制SKOV3细胞增殖,诱导其凋亡,72h IC50约为6μmol/L。其诱导凋亡机制可能与Bax的上调和Bcl-2的下调相关。Objective: To investigate the effects of arsenic trioxide on ovarian cancer cell line SKOV3 and its mechanism. Methods: Growth inhibition/apoptosis and cell cycles changes of SKOV3 cell line induced by arsenic trioxide were measured by means of MIT/flow cytometry/elec-tronic microscope. RT-PCR technique was used to investigate the transcriptional changes of gene P53/Bax/Bcl-2.Results: (1)The growth inhibition of SKOV3 cell line induced by arsenic trioxide was enhanced in time-dependent and dose-dependent pattern and IC50 of 72 hours was 6μmol/L; (2)Apoptosis was detected by electronic microscope/flow cytometry. At the same time G2/M retardation was founded. (3)RT-PCR showed that arsenic trioxide induced up regulation of Bax and down regulation of Bcl-2.Conclusions:In vitro arsenic trioxide can inhibit the growth of SKOV3 cell line and induce apoptosis.The IC50 of 72 hours is 6umol/L. Its mechanism may correlate with the up-regulation of Bax and down-regulation of Bcl-2.
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