摘要
目的探索茶多酚EGCG对人肝癌细胞HepG2中LDL的摄取情况的影响及其可能的分子机制。方法培养人肝癌细胞HepG2细胞,茶多酚EGCG刺激HepG2细胞,用Real-time PCR和western blot的方法分别检测LDLR的mRNA和蛋白水平表达以及核内蛋白SREBP2的表达情况。用DiI-LDL染色的方法检测LDL的摄取情况。另外,利用RNAi技术进一步检测SREBP2对LDLR的表达和LDL的摄取情况。结果 EGCG可增加LDLR的mRNA(P<0.05)和蛋白水平(P<0.01)的表达以及核内SREBP2(P<0.01)的表达,可明显促进LDL的摄取。转染SREBP2的小干扰RNA后,可明显抑制EGCG引起的LDLR的表达(P<0.01)及LDL的摄取。结论从细胞水平证明茶多酚EGCG可通过激活SREBP2/LDLR通路促进LDL的摄取。
Objective To clarify the molecular mechanism of the effect of EGCG on LDL uptake in HepG2 cells.Methods HepG2 cells were cultured and treated with EGCG.Treatment of HepG2 cells with EGCG.The mRNA expression of LDLR was analyzed by Real-time PCR.The protein levels of LDLR and nuclear SREBP2 were detected by western blotting.DiI-LDL assay was employed to examine the LDL uptake.In addition,cells were transfected with small infereing RNA（siRNA） of SREBP2 to observe the role of SREBP2 in the up-regulation of LDLR expression and LDL uptake induced by EGCG.Results EGCG promotes the mRNA expression of LDLR（P〈0.05）,protein expression of LDLR（P〈0.01） and nuclear SREBP2（P〈0.01）.Further,EGCG enhanced LDL uptake.Transfected the cells with SREBP2 siRNA,the data showed that the SREBP2 siRNA could block the expression of LDLR（P〈0.01） and LDL uptake.Conclusion EGCG promotes LDL uptake through SREBP2/LDLR pathway in HepG2 cells.
作者
郭琳娜
孙静
崔传珏
李建军
GUO Lin-na1, SUN ,ling2, CUI Chuan-jue1, LI Jian-jun1,2(1.State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beil＇ing 100037, China. 2. Division of Dyslipidemia, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Center for Cardiovascular Diseases, Beijing 100037, China)
出处
《中国分子心脏病学杂志》
CAS
2018年第4期2581-2584,共4页
Molecular Cardiology of China
基金
国家自然科学基金青年基金项目(81600680)
