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出 处:《中国比较医学杂志》2011年第6期6-11,87,共7页Chinese Journal of Comparative Medicine
基 金:南京军区医学科技研究"十一五"计划课题资助(07Z034);福建省自然科学基金(2010J01221)
摘 要:目的本实验以小鼠T细胞淋巴瘤细胞株EL-4细胞株为模型,研究淫羊藿素(icaritin,ICT)是否抑制瘤细胞增殖,并初步探讨其作用机制。方法应用MTT比色法、透射电镜技术及流式细胞术检测ICT对EL-4细胞增殖能力的影响;用RT-PCR技术、比色法分析ICT的作用机制。结果 ICT对EL-4细胞增殖具有明显抑制作用,并呈量效及时效关系。透射电镜及流式细胞术结果显示,ICT可诱导EL-4细胞凋亡。RT-PCR显示,ICT作用于EL-4细胞后,bcl-2、P21基因的mRNA表达下调,Caspase-3、Caspase-9酶活性显著增强。结论 ICT可抑制体外培养的小鼠T淋巴瘤EL-4细胞的增殖并诱导其凋亡,可能系通过下调bcl-2、P21 mRNA表达,激活Caspase-3、Caspase-9蛋白等途径实现的。Objective To investigate the effect and probable mechanism of icaritin(ICT) on EL-4 cells in vitro.Methods MTT、transmission electron microscope(TEM)、flow cytometry analysis were used to examine the effect of ICT on the proliferation of EL-4 cells.Reverse transcript-polymerase chain reaction(RT-PCR) assay and colorimetric method was used to reveal the probable mechanism.Results ICT could inhibit the proliferation of EL-4 cells significantly in a dose-and time-dependent manner.Apoptotic cells were observed by TEM and flow cytometry analysis.RT-PCR analysis showed that the expression of bcl-2、P21 were down-regulated.Besides,Caspase-3 and Caspase-9 activity in EL-4 cells elevated remarkably.Conclusions ICT could inhibit the proliferation of EL-4 cells and induce EL-4 cells apoptosis in vitro.The probable mechanism may be down-regulate the expression of bcl-2、P21and elevate Caspase-3 and Caspase-9 activity in EL-4 cells.
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