染料木黄酮对油酸诱导脂肪变HepG2细胞PPARα表达和糖脂水平的影响  

EFFECT OF GENISTEIN ON THE CHANGES OF PPARα EXPRESSION AND GLYCOLIPID LEVEL IN OLEIC ACID-INDUCED STEATOSIS IN HEPG2 CELLS

作　　者：候舒舰 吴丹[1] 蒋卓勤[1] 

机构地区：[1]中山大学公共卫生学院广东省营养膳食与健康重点实验室,广州510080

出　　处：《营养学报》2014年第1期49-52,共4页Acta Nutrimenta Sinica

基　　金：广东省自然科学基金(No.10151008901000063)

摘　　要：目的研究染料木黄酮（genistein，Gen）对油酸（oleic acid，OA）诱导脂肪变HepG2细胞的过氧化物酶体增殖物激活受体α（peroxisome proliferators—activatedreceptor α，PPARα）蛋白表达和糖、脂代谢水平的影响。方法将HepG2细胞在合有0～50gmol／L的Gen，0．5mmol／L的OA的培养基内，且设置对照组，培养24h后收集细胞，分别采用蛋白质印迹法（Western blotting）、酶法、选择性沉淀法测定PPARα、总胆固醇（TC）、高密度脂蛋白胆固醇（HDL—C）的含量；收集培养基上清液，采用葡萄糖氧化酶-过氧化物酶法测定葡萄糖消耗量。结果浓度为10～50μmol／L的Gen可以减轻HepG2细胞脂肪变的程度，总体上呈现剂量效应关系。Gen各组与模型组比较，高浓度的Gen（50,mol？L）可有效提高OA诱导脂肪变HepG2细胞内PPARα和HDL—C含量，降低TC和葡萄糖消耗量，但低浓度的Gen（10-30μmol／L）对细胞内TC和HDL—C作用不明显。结论高浓度Gen能改善OA诱导的脂肪变HepG2细胞内的糖脂代谢情况，并可能与PPARα表达有关。Objective To study the effect of genistein （Gen） on the contents of peroxisome proliferator-activated receptor α（PPARα） and glycolipids in oleic acid （OA）-induced steatosis in HepG2 cell. Methods HepG2 cells were treated with 0-50btmol/L Gen, 0.5 mmol/L OA. A control group was set. The cells were collected after 24 h. The contents of PPARα, total cholesterol （TC） and high density lipoprotein-cholesterol （HDL-C） were determined by Western blotting, enzymic method and selective precipitation sequentially. The supernatants were collected in the meantime and the consumption of glucose was measured by glucose oxidase-peroxide enzyme. Results Gen co-treatment（ 10-50μmol/L）significantly alleviated fatty degeneration dose-dependently. Compared with model group, PPARα, HDL-C were improved significantly in the high-dose group （50μmol/L）. TC and glucose consumption were lowered significantly. But the contents of TC and HDL-C were not changed obviously in the low-dose group （10-30μmol/L）. Conclusion Gen can protect against OA-induced steatosis in HepG2 cells by alleviating the disorder of glycolipid metabolism, and increasing PPARα expression.

关 键 词：染料木黄酮 脂肪变HepG2细胞 PPARα糖脂代谢 

分 类 号：R96[医药卫生—药理学]