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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 (FF) on triglyceride metabolism and oxidative stress in fatty liver cells. Methods HepG2 cells were induced by oleic acid (OA) to induce steatosis in HepG2 cells. The HepG2 cells were treated with different concentrations of FF (0, 5, 10 and 50 μmol / L) 3-phosphate oxidase method was used to detect intracellular triglyceride (TG) content, thiobarbituric acid colorimetric method and xanthine oxidase method were used to determine the content of malondialdehyde (MDA) in cell culture supernatant and Superoxide dismutase (SOD) activity. Results OA induced hepatic steatosis in HepG2 cells, and the intracellular TG content increased significantly. At the same time, the content of MDA in cell culture supernatant increased and the activity of SOD decreased. FF could obviously reduce the fatty degeneration of HepG2 cells induced by oleic acid, The supernatant MDA content, improve SOD activity. Conclusion Fenofibrate inhibits oleic acid-induced steatosis of HepG2 cells, which may be related to the enhancement of anti-oxidative ability and the reduction of oxidative stress in HepG2 cells.