title: [Protective effects of antioxidants on chronic intermittent hypoxia-induced cardiac remodeling in mice].
abstract: OBJECTIVE
  Chronic intermittent hypoxia (CIH) animal model was used to mimic the status of obstructive sleep apnea (OSA) in order to investigate the pathological mechanism of CIH-induced cardiac remodeling and observe the protective effect of antioxidants.
  
  
  METHODS
  FVB mice (8-10 weeks-old) were randomly divided into control (saline, i.p.) group and CIH group, reduced form of nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin (APO, 3 mg×kg(-1)×d(-1), i.p.) alone or CIH+APO, SOD mimic MnTMPyP (SODM, 5 mg×kg(-1)×d(-1), i.p.) alone or CIH+SODM (n = 5 each). After 4 weeks, cardiac function and structure were determined by echocardiography, cardiac inflammation, apoptosis, cardiac fibrosis and cardiac MDA contents were examined by Western blot and chemical-biological methods, respectively.
  
  
  RESULTS
  (1) Heart weight, LVIDd and LVIDs were increased while LVEF and FS were reduced in CIH group compared to control group (all P < 0.05). (2) Myocardial protein expression of ANP and VCAM-1 was significantly upregulated, myocardial MDA content and apoptosis as well as myocardial fibrosis marker CTGF and PAI-1 were increased in CIH group compared to control group (all P < 0.05). (3) Above parameters were similar between APO and CIH+APO as well as SODM and CIH+SODM (all P > 0.05).
  
  
  CONCLUSIONS
  CIH could induce cardiac remodeling and CIH-induced cardiac inflammation, cardiac oxidative injury, cardiac apoptosis and cardiac fibrosis serve as the pathological mechanisms of CIH-induced cardiac remodeling. The protective effects of the two antioxidants suggest that the main mechanism of CIH-induced cardiac injury is oxidative stress.
authors.affiliation: Clinic Center of Cardiovascular Department, First Hospital, Jilin University, Changchun 130021, China.
authors.forename: Xia
authors.initials: X
authors.lastname: Yin
authors.affiliation: Clinic Center of Cardiovascular Department, First Hospital, Jilin University, Changchun 130021, China.
authors.forename: Baicheng
authors.initials: B
authors.lastname: Li
authors.affiliation: Clinic Center of Cardiovascular Department, First Hospital, Jilin University, Changchun 130021, China.
authors.forename: Yuguang
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: Clinic Center of Cardiovascular Department, First Hospital, Jilin University, Changchun 130021, China.
authors.forename: Weixia
authors.initials: W
authors.lastname: Sun
authors.affiliation: Clinic Center of Cardiovascular Department, First Hospital, Jilin University, Changchun 130021, China. Email: zhengyanghappy07@sina.com.
authors.forename: Yang
authors.initials: Y
authors.lastname: Zheng
mesh_terms: D000098:Acetophenones; D000818:Animals; D000975:Antioxidants / Q000502:physiology*; D017209:Apoptosis; D004195:Disease Models, Animal; D006321:Heart; D000860:Hypoxia; D051379:Mice; D008815:Mice, Inbred Strains; D009206:Myocardium; D019255:NADPH Oxidases; D018384:Oxidative Stress; D017395:Plasminogen Activator Inhibitor 1 / Q000096:biosynthesis; D020181:Sleep Apnea, Obstructive / Q000150:complications*; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis; D066253:Vascular Remodeling
chemical_list: D000098:Acetophenones; D000975:Antioxidants; D017395:Plasminogen Activator Inhibitor 1; D019010:Vascular Cell Adhesion Molecule-1; C056165:acetovanillone; D019255:NADPH Oxidases