RESUMO
Objective: To explore the effect and mechanism of genistein on oleic acid-induced lipid accumulation in HepG2 cells. Method: Lipid accumulation model in HepG2 cells was induced by different concentrations of oleic acid for 24 h, and 12.5, 25, 50 μmol·L-1genistein and oleic acid acted on cells for 24 h. Cell viability was determined by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay. Double staining with Nile red and DAPI was used to observe the intracellular lipid droplets. Intracellular triglyceride (TG) content was determined by kit. The protein expression levels of triglyceride lipase(ATGL),hormone-sensitive fatty acid(HSL),phosphorylation HSL(p-HSL),silent information regulator 1(STRT1),peroxisome proliferator-activated receptor α(PPARα),carnitine palmityl transferase 1(CPT-1) in oleic acid-induced HepG2 cells were detected by Western blot. Result: 0.5 mmol·L-1 oleic acid and 12.5, 25, 50 μmol·L-1 genistein had no significant effect on cell viability after treated cells for 24 h. Compared with normal group, the TG content and lipid droplets in oleic acid-induced HepG2 cells was significantly increased (PPPPα, and CPT-1 compared with model group (PPConclusion: Genistein can significantly improve the lipid accumulation in oleic acid-induced HepG2 cells, and its mechanism may be related to up-regulating the protein expression levels of ATGL, p-HSL/HSL, SIRT1, PPARα, CPT-1, and thus promoting lipid hydrolysis and oxidative metabolism.