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作 者:吴丹[1] 邓颖勋[1] 王宇琦[1] 黎虎[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510030
出 处:《营养学报》2013年第4期353-356,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)诱导的脂肪变HepG2细胞胞核内Lipin1水平以及培养基和胞浆内甘油三酯水平的影响。方法在HepG2细胞中分别或联合加入0~640μmol/L的Gen,0~2.0 mmol/L的OA干预,用MTT法测定细胞活性,以确定适宜的OA建模和Gen的干预浓度。之后,采用OA建立HepG2细胞脂肪变模型,用Gen干预24h,收集培养基上清和细胞分别测定甘油三酯水平,Western blot检测胞核Lipin1的表达。结果 0.5 mmol/L OA为造模最佳干预浓度,可同时提高培养基和细胞中甘油三酯的含量,10~50 mol/L的Gen可以减轻HepG2细胞脂肪变的状态,并且呈现剂量效应关系(P<0.05),同时,胞核内Lipin1水平增加(P<0.05)。结论 Gen能抑制OA诱导的HepG2细胞脂肪变,并可能与Lipin1的核转移有关。Objective To observe the effect of genistein (Gen) on nuclear Lipin 1 expression and triglyceride content in both cytoplasm and culture medium in oleic acid (OA)-induced steatosis in HepG2 cells. Methods HepG2 cells were treated with 0-640p, mol/L Gen or 0-2.0 mmol/L OA respectively or simultaneously. Then, the cell activity was detected by MTT. OA induced steatosis model and the appropriate Gen intervention were developed. Afterwards, OA induced steatosis was intervened with Gen for 24 h, followed by determination of triglyceride levels (TG) in medium and cytoplasm and the nuclear Lipinl expression in HepG2 cells by Western blotting. Results OA at 0.5 mmol/L successfully induced HepG2 cell steatosis by increasing TG levels both in medium and cytoplasm. However, Gen co-treatment ( 10-50μmol/L) significantly alleviated the above phenomenon dose-dependently (P〈0.05), and accompanied by increased nuclear Lipinl expression in HepG2 cells (P〈0.05). Conclusion Gen can protect HepG2 cells against OA-induced steatosis, and the underlying mechanism may involve in Lipin 1 nuclear translocation.
关 键 词:染料木黄酮 甘油三酯 HEPG2细胞 Lipin1
分 类 号:R151[医药卫生—营养与食品卫生学]
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