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机构地区:[1]山西医科大学第一医院感染病科,太原030001
出 处:《中国医疗前沿》2011年第23期4-5,共2页China Healthcare Innovation
基 金:山西省2009年人才引进与开发专项资金(编号:08159)
摘 要:目的探讨非诺贝特(fenofibrate,FF)对脂肪变性肝细胞甘油三酯代谢及氧化应激水平的影响。方法以油酸(OA)诱导人肝癌HepG2细胞脂肪变性为模型,采用不同浓度的FF(0、5、10、50μmol/L)干预HepG2细胞24h,油红O染色观察HepG2细胞内脂滴,甘油-3-磷酸氧化酶法检测细胞内甘油三酯(TG)含量,硫代巴比妥酸比色法、黄嘌呤氧化酶法分别测定细胞培养上清液中的丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。结果 OA诱导HepG2细胞脂肪变性,细胞内TG含量明显增加,同时细胞培养上清液中MDA含量增加,SOD活性降低;FF能明显减轻油酸诱导的HepG2细胞脂肪变性,降低细胞内TG水平及细胞培养上清液中MDA含量,提高SOD活性。结论非诺贝特抑制油酸诱导的HepG2细胞脂肪变性,其可能与提高HepG2细胞的抗氧化能力、减轻细胞氧化应激损害有关。Objective To investigate the Effects of fenofibrate on the triglyceride metabolism and Oxidative Stress in steatotic HepG2 cells.Methods A steatotic hepatocytes model was established by treating HepG2 cells with oleic acid,the cells were treats with different concentrations of fenofibrate for 24 hours.Significant fat accumulation was documented by Oil Red Ostaining,and intracellular triglyceride levels was detected by triglyceride enzymatic assay.The level of Malondialdehyde and Superoxide Dismutase were assayed by thibabituric acid method,xanthine oxidase method.Results After incubation with OA for 24 hours,the TG deposition of HepG2 in the model group increased markedly,and TG content was 379.98±23.19mg/g protein(P〈0.05),at the same time,The elevation of MDA content was detected,however,SOD reduced remarkably(P〈0.05).FF(5,10,50μmol/L) inhibited the HepG2 cells steatosis induced by OA in a concentration-dependent manner,FF decreased TG and MDA content significantly(P〈0.05),while the SOD activity significantly increased(P〈0.05).Conclusion FF prevents OA-induced HepG2 cells steatosis,and it may be related to raise the anti-oxidation ability,reduce the oxidation stress.
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