title: [Effects of PPAR-alpha activation on oleic acid-induced steatosis and expression of heme oxygenase-1 in HepG2 cells].
abstract: OBJECTIVE
  To investigate the effects of peroxisome proliferator activated receptor-alpha (PPAR-a) activation on oleic acid (OA)-induced steatosis and hepatic expression of heme oxygenase-1 (HO-1) using an in vitro cell model system.
  
  
  METHODS
  A steatosis human hepatocyte in vitro model system was established by treating HepG2 cells with 0.2 mmol/L of oleic acid for 24 hours. The steatosis cells were then divided into four groups for an additional 24 hours of treatment with 0.2 mmol/L of oleic acid alone (model control group) or with 5, 10 or 50 pnol/L of fenofibrate (FF, a selective PPAR-a agonist; experimental groups). Untreated HepG2 cells served as non-steatosis controls. Effect of PPAR-a activation on fat accumulation was detected by Oil Red O staining and on intracellular triglyceride (TG) levels by enzymatic assay. mRNA and protein expression of PPAR-alpha and HO-1 were quantified by real-time PCR and immunocytochemistry, respectively. One-way ANOVA and the LSD t-test were used for between-group comparisons, and correlation analysis was performed with the Pearson's correlation coefficient.
  
  
  RESULTS
  The steatosis model control cells showed significantly increased TG deposition (379.98 +/- 23.19 mg/g protein, vs. non-steatosis controls F = 148.56, P< 0.01), significantly decreased mRNA and protein expression of PPAR-alpha (0.42 +/- 0.38,F= 177.64,P< 0.01 and 0.47 +/- 0.14, F= 120.76,P< 0.01) and HO-1 (0.36 +/- 0.66, F= 74.77,P< 0.01 and 0.26 +/- 0.10,F= 119.90,P<0.01). FF (5, 10 and 50 micromol/L) inhibited the steatosis induced by OA in a concentration-dependent manner (294.00 +/- 19.80, 250.33 +/- 9.96, and 196.99 +/- 9.14, F = 148.56, P <0.01) and increased the mRNA and protein expression of PPAR-alpha (0.55 +/- 0.65, 0.85 +/- 0.61, and 1.31 +/- 0.36,F= 177.64,P< 0.01; 0.82 + 0.11, 1.31 +/- 0.16, and 1.75 +/- 0.13, F= 120.76,P <0.01) and HO-1 (0.62 +/- 0.05, 0.84 +/- 0.07, and 1.30 +/- 0.11,F= 74.77,P <0.01; 0.44 +/- 0.08, 0.81 +/- 0.08, 1.20 +/- 0.10,F= 119.90,P< 0.01).
  
  
  CONCLUSIONS
  Activation of PPAR-a prevents OA-induced steatosis in HepG2 cells, and HO-1 may function as a downstream effector of this mechanism.
authors: Department of Infectious Disease, the First Hospital of Shanxi Medical University, Taiyuan 030001, China.
authors: Jing-jing
authors: JJ
authors: Zhao
authors: Long-feng
authors: LF
authors: Zhao
authors: Hui
authors: H
authors: Yang
authors: Li
authors: L
authors: Zhang
mesh_terms: D005234:Fatty Liver / Q000139:chemically induced; D051547:Heme Oxygenase-1 / Q000378:metabolism*; D056945:Hep G2 Cells; D006801:Humans; D019301:Oleic Acid / Q000494:pharmacology*; D047493:PPAR alpha / Q000378:metabolism*; D014280:Triglycerides / Q000378:metabolism
chemical_list: D047493:PPAR alpha; D014280:Triglycerides; D019301:Oleic Acid; C496541:HMOX1 protein, human; D051547:Heme Oxygenase-1