title: Adiponectin abates atherosclerosis by reducing oxidative stress.
abstract: BACKGROUND
  We investigated whether the anti-atherosclerosis of adiponectin (APN) relates to the reduction of oxidative stress. We observed the overexpression of adiponectin gene with different titers on atherosclerosis (AS) models of high-fat apolipoprotein E-deficient (ApoE-/-) mice.
  
  
  METHODS
  We divided 48 male ApoE-/- mice into 4 groups: control group, high-fat diet group, low adiponectin group, and high adiponectin group. The low and high adiponectin group mice were treated with recombinant adenovirus expressing mice adiponectin (Ad-APN) with low-dose adiponectin 1.0×108 p.f.u. and high-dose adiponectin 5.0×108 p.f.u. via the tail every 2 weeks and given a high-fat diet for the last 8 weeks. On the 14th day after injection, blood samples were obtained from the vena cava.
  
  
  RESULTS
  Along with increased serum adiponectin, serum superoxide dismutase (SOD) activity increased (P<0.05) and concentration of malondialdehyde (MDA) was decreased (P<0.05). Levels of total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) were decreased, especially TC and LDL-C (P<0.05). A real-time fluorescent quantitative polymerase chain reaction test was used to analyze levels of mRNA expression for endothelial nitric oxide synthase (eNOS) and adiponectin in the aorta. Along with increased adiponectin, the mRNA expression of eNOS in the aorta was increased significantly (P<0.05). The lesion formation in the aortic sinus was inhibited by 25% and 31% in the low-APN group and high-APN group, respectively (P<0.05). Along with the increase of adiponectin doses, the damage of atherosclerosis gradually eased. However, the differences between the low-APN group and high-APN group had no statistical significance.
  
  
  CONCLUSIONS
  Adiponectin may protect the aorta from atherosclerosis injury by reducing oxidative stress, reducing lesion formation size in the aortic root and reducing TC, TG, and LDL-C in serum. The molecular mechanism may involve preservation of SOD, reducing MDA in serum, and increasing eNOS and adiponectin mRNA expression in the aorta.
authors.affiliation: Xinjiang Key Laboratory of Medical Animal Model Research, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
authors.forename: Xuemei
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Science and Research Education Center, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
authors.forename: Hongwei
authors.initials: H
authors.lastname: Pu
authors.affiliation: Department of Micro-Reconstructive Surgery of Orthopedics Center, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
authors.forename: Chuang
authors.initials: C
authors.lastname: Ma
authors.affiliation: Xinjiang Key Laboratory of Medical Animal Model Research, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
authors.forename: Tao
authors.initials: T
authors.lastname: Jiang
authors.affiliation: Xinjiang Key Laboratory of Medical Animal Model Research, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
authors.forename: Qin
authors.initials: Q
authors.lastname: Wei
authors.affiliation: Xinjiang Key Laboratory of Medical Animal Model Research, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
authors.forename: Chun
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Xinjiang Key Laboratory of Medical animal Model Research, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
authors.forename: Mingjun
authors.initials: M
authors.lastname: Duan
authors.affiliation: Xinjiang Key Laboratory of Medical Animal Model Research, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
authors.forename: Xi
authors.initials: X
authors.lastname: Shou
authors.affiliation: College of Basic Medicine, Xinjiang Medical University, Urumqi, China (mainland).
authors.forename: Lipin
authors.initials: L
authors.lastname: Su
authors.affiliation: College of Basic Medicine, Xinjiang Medical University, Urumqi, China (mainland).
authors.forename: Jianlong
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
authors.forename: Yining
authors.initials: Y
authors.lastname: Yang
mesh_terms: D052242:Adiponectin / Q000235:genetics / Q000502:physiology*; D000818:Animals; D050197:Atherosclerosis / Q000378:metabolism / Q000503:physiopathology*; D001483:Base Sequence; D017931:DNA Primers; D004195:Disease Models, Animal; D008297:Male; D051379:Mice; D018384:Oxidative Stress; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000235:genetics
chemical_list: D052242:Adiponectin; D017931:DNA Primers; D012333:RNA, Messenger