title: Curcumin decreases oleic acid-induced lipid accumulation via AMPK phosphorylation in hepatocarcinoma cells.
abstract: OBJECTIVE
  Non-alcoholic fatty liver disease (NAFLD) is one of the most common metabolic syndromes and is characterized by the accumulation of hepatic triglycerides (TG), which result from an imbalance between uptake, synthesis, export, and oxidation of fatty acids. Curcumin is a polyphenol derived from the herbal remedy and dietary spice turmeric, was found to prevent obesity and diabetes in mouse models. However, a hypolipidemic effect of curcumin in oleic acid- induced hepatocarcinoma cells has not been reported. In this study, we examined the effect of curcumin on reducing lipid accumulation in hepatic cells.
  
  
  METHODS
  Hepatocytes were treated with oleic acid (OA) containing with or without curcumin to observe the lipid accumulation by Oil Red O stain. We also tested the effects of curcumin on triglycerides (TG) and total cholesterol (TC) in HepG2 cells. Western blot and reverse transcription polymerase chain reaction (RT-PCR) was used to measure sterol regulatory element binding proteins-1 (SREBP-1), fatty acid synthase (FAS), peroxisome proliferator-activated receptor (PPAR)-α, and adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) expression.
  
  
  RESULTS
  Curcumin suppressed OA-induced lipid accumulation and TG and TC levels. Also, curcumin decreased hepatic lipogenesis such as SREBP-1, and FAS. Besides, we also found out the antioxidative effect of curcumin by increasing the expression of PPARα. Curcumin increased AMPK phosphorylation in hepatocytes.
  
  
  CONCLUSIONS
  These results indicated that curcumin has the same ability to activate AMPK and then reduce SREBP-1, and FAS expression, finally leading to inhibit hepatic lipogenesis and hepatic antioxidative ability. In this report, we found curcumin exerted a regulatory effect on lipid accumulation by decreasing lipogenesis in hepatocyte. Therefore, curcumin extract may be active in the prevention of fatty liver.
authors.affiliation: Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University, Wonkwang Oriental Medicines Research Institute, Institute of Biotechnology, Iksan, Jeonbuk, Republic of Korea. sssimi@wonkwang.ac.kr  
authors.forename: O H
authors.initials: OH
authors.lastname: Kang
authors.forename: S B
authors.initials: SB
authors.lastname: Kim
authors.forename: Y S
authors.initials: YS
authors.lastname: Seo
authors.forename: D K
authors.initials: DK
authors.lastname: Joung
authors.forename: S H
authors.initials: SH
authors.lastname: Mun
authors.forename: J G
authors.initials: JG
authors.lastname: Choi
authors.forename: Y M
authors.initials: YM
authors.lastname: Lee
authors.forename: D G
authors.initials: DG
authors.lastname: Kang
authors.forename: H S
authors.initials: HS
authors.lastname: Lee
authors.forename: D Y
authors.initials: DY
authors.lastname: Kwon
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D006528:Carcinoma, Hepatocellular / Q000378:metabolism*; D003474:Curcumin / Q000494:pharmacology*; D056945:Hep G2 Cells; D006801:Humans; D050356:Lipid Metabolism / Q000187:drug effects*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008113:Liver Neoplasms / Q000378:metabolism*; D019301:Oleic Acid / Q000494:pharmacology*; D010766:Phosphorylation; D051780:Sterol Regulatory Element Binding Protein 1 / Q000502:physiology; D014280:Triglycerides / Q000097:blood
chemical_list: C497387:SREBF1 protein, human; D051780:Sterol Regulatory Element Binding Protein 1; D014280:Triglycerides; D019301:Oleic Acid; D055372:AMP-Activated Protein Kinases; D003474:Curcumin