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芬维A胺通过抑制ERK1/2活化促进人肝癌细胞凋亡 被引量:5

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摘要 目的:探讨芬维A胺对人肝癌细胞凋亡的影响及其可能机制。方法:用芬维A胺(10μmol/L)处理人肝癌细胞株(SNU475,SNU449,SNU182,SK-HEP-1,PLC/PRF/5),通过CellTiter-Glo发光细胞活力检测试剂盒和Caspase-3/7检测试剂盒检测芬维A胺的凋亡效应;通过实时定量PCR检测核受体Nur77、维甲酸受体β(retinoic acid receptor,RARβ)mRNA的变化;并用Western-blot检测细胞ERK1/2蛋白的激活情况。结果:芬维A胺处理24h能诱导SK-HEP-1、PLC/PRF/5细胞凋亡;但对SNU475、SNU449、SNU182细胞凋亡影响不显著(P>0.05)。在敏感的SK-HEP-1、PLC/PRF/5细胞中,芬维A胺显著降低ERK1/2蛋白活化,但对核受体Nur77、RARβmRNA表达无显著影响。结论:芬维A胺体外诱导人肝癌SK-HEP-1、PLC/PRF/5细胞凋亡可能通过抑制ERK1/2蛋白活化起作用。
出处 《实用医学杂志》 CAS 北大核心 2012年第18期3006-3008,共3页 The Journal of Practical Medicine
基金 国家自然青年基金(编号:81001109) 广州市教育局"羊城学者青年学术骨干培养项目"(编号:10A015G) 广东省医学科研基金(编号:A2012253) 广州医学院博士启动项目[编号:2010(06)]
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