摘要
目的研究大黄素对多药耐药白血病细胞株K562/Adr(KAR)增生、凋亡的影响及探讨bcr-abl、mdr-1基因在其中的变化。方法应用四甲基偶氮唑蓝(MTT)比色法、DNA片段化分析及TdT酶介导的末端缺失原位标记(TUNEL)法检测大黄素对KAR细胞增生及凋亡的影响;RT-PCR法检测大黄素对KAR细胞bcr-abl、mdr-1基因mRNA表达的影响;Western blotting法检测大黄素对KAR细胞bcr-abl融合蛋白P210表达的影响。结果大黄素能有效抑制KAR细胞的增生,作用72 h的IC_(50)约为20μmol/L,并能诱导其凋亡,随药物作用浓度的增加,凋亡率也逐渐上升;大黄素下调KAR细胞bcr-abl、mdr-1基因mRNA的表达;也下调了KAR细胞P210蛋白的表达。结论大黄素能有效抑制KAR细胞增生,诱导其凋亡;并可能通过下调bcr-abl和mdr-1的表达起作用。
Objective To investigate the effects of emodin on proliferation inhibition and apoptosis induction in multidrug resistant leukemia cell line K562/Adr (KAR) and on expressions of bcr-abl,mdr-1 genes.Methods KAR cells were exposed to various dosages of emodin.MTT assay was used to detect KAR cell proliferation.The ability of Emodin to induce apoptosis of KAR cells was examined by DNA fragmentation analysis and detection of TdT mediated dUTP nick end labeling (TUNEL).The expressions of bcr-abl and mdr-1 mRNA were studied by reverse transcription-polymerase chain reaction (RT-PCR) and bcr-abl fusion protein P210 by Western blotting.Results The results showed that Emodin could remarkably inhibit the cell proliferation,and the IC_(50) value for 72 h of treatment was about 20μmol/L.Apoptosis in KAR cells could be induced by emodin in a dose dependent manner.The expressions of bcr-abl and mdr-1 mRNA and P210 protein decreased in KAR cells treated with Emodin.Conclusion Emodin could efficiently inhibit cell growth and induce apoptosis in KAR cells,in which down-regulation of bcr-abl and mdr-1 expressions may involve.
出处
《白血病．淋巴瘤》
CAS
2007年第3期176-179,共4页
Journal of Leukemia & Lymphoma
基金
福建省科技三项费用基金(2002Y048)
福建省医学创新课题基金(2001CX02)
福建医科大学教授基金(闽医大2006187)
