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作 者:许君[1] 高振兴[1] 马倩[1] 张玉娟[1] 史磊[1] 郑文明[1]
出 处:《营养学报》2012年第4期368-372,共5页Acta Nutrimenta Sinica
基 金:河南农业大学博士专项基金(No.30200274)
摘 要:目的验证不同儿茶素单体对HBV的抑制作用,并初步研究对其抗乙型肝炎病毒的分子机制。方法采用稳定表达乙型肝炎病毒(hepatitis B virus,HBV)表面抗原和E抗原的HepG2.2.15细胞系,不同浓度的儿茶素作用于细胞后,ELISA分析HBsAg和HBeAg的表达;以影响HBV转录的几个关键肝富集转录因子(liver-enriched transcription factors,LETFs)为对象,RT-PCR分析转录水平上,不同浓度的表没食子儿茶素没食子酸酯(epigallocatechin gallate,EGCG)对HepG2.2.15细胞的关键LETFs的表达影响。结果几种儿茶素单体中,EGCG的抗HBV效果最明显;EGCG可明显下调视黄醇X受体α(retinoid X receptorα,RXRα)和胆汁酸受体(farnesoid X receptorα,FXRα)的表达。结论EGCG的抗HBV作用的分子机制可能与其下调HBV转录的关键肝富集转录因子RXRα和FXRα有关。Objective To validate the anti-hepatitis B virus(HBV) effects of green tea catechins and its molecular mechanism.Methods ELISA analysis of HBsAg and HBeAg in culture supernant was performed after HepG2.2.15 cell was treated with different concentration of green tea catechins.Semi-quantitative RT-PCR analysis was applied to study the expression of several key LETFs which influenced transcription and replication of HBV genome of HepG2.2.15 post-treatment with EGCG.Results EGCG was the optimal anti-HBV component among treated catechins.EGCG down-regulated the expression of retinoid X receptor α(RXRα) and farnesoid X receptor α(FXRα) significantly.Conclusion The anti-HBV molecular mechanism of EGCG may be associated with downregulation of two key liver-enriched transcription factors RXRα and FXRα.
关 键 词:EGCG HBV 肝富集转录因子 HEPG2.2.15
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