title: [Statin reduced triglyceride level via activating peroxisome proliferator activated receptor α and upregulating apolipoprotein A5 in hypertriglyceridemic rats].
abstract: OBJECTIVE
  to explore the potential role of apolipoprotein A5 (apoA5) on the hypertriglyceridemia (HTG)-lowering effects of statin.
  
  
  METHODS
  twenty-four Sprague-Dawley rats were randomized into 3 groups: (1) control group (n = 8), with no special treatment; (2) HTG group (n = 8), treated with 10% fructose water for 6 weeks; (3) statin group (n = 8), treated with 10% fructose water for 2 weeks and cotreated with atorvastatin 10 mg×kg(-1)×d(-1) for another 4 weeks. Body weight, fasting plasma lipids and the hepatic expressions of apoA5 and peroxisome proliferator activated receptor (PPAR)α were determined. In separate in vitro experiments, we tested the effects of atorvastatin on TG and the expressions of apoA5 and PPARα in HepG2 cells.
  
  
  RESULTS
  (1) at 6 weeks, plasma TG was higher in rats in HTG group than in controls, which was significantly reduced in statin group (both P < 0.05). (2) Rat hepatic apoA5 expression in HTG group was significantly lower than in control group and was significantly higher in statin group than in HTG group (both P < 0.05). (3) Similarly, rat PPARα mRNA expression in HTG group was lower than in control group and was higher in statin group than in HTG group (both P < 0.05). (4) Statin significantly upregulated the expressions of apoA5 and PPARα and decreased TG in HepG2 cells. The above effects induced by statin was blocked in the presence of PPARα inhibitor.
  
  
  CONCLUSIONS
  upregulation of apoA5 expression contributes to TG lowering effect of statin via PPARα signaling pathway.
authors.affiliation: Department of Cardiology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
authors.forename: Xian-sheng
authors.initials: XS
authors.lastname: HUANG
authors.forename: Shui-ping
authors.initials: SP
authors.lastname: ZHAO
authors.forename: Lin
authors.initials: L
authors.lastname: BAI
authors.forename: Qian
authors.initials: Q
authors.lastname: ZHANG
authors.forename: Min
authors.initials: M
authors.lastname: HU
authors.forename: Wang
authors.initials: W
authors.lastname: ZHAO
mesh_terms: D000818:Animals; D000072040:Apolipoprotein A-V; D001053:Apolipoproteins / Q000097:blood*; D000069059:Atorvastatin; D015536:Down-Regulation; D056945:Hep G2 Cells; D006538:Heptanoic Acids / Q000494:pharmacology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D015228:Hypertriglyceridemia / Q000378:metabolism*; D008297:Male; D047493:PPAR alpha / Q000378:metabolism*; D011758:Pyrroles / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000097:blood*; D015854:Up-Regulation
chemical_list: C514818:Apoa5 protein, rat; D000072040:Apolipoprotein A-V; D001053:Apolipoproteins; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D047493:PPAR alpha; D011758:Pyrroles; D014280:Triglycerides; D000069059:Atorvastatin