title: [Protective effect of oxymatrine on chronic heart failure and ADMA metabolism pathway in isoproterenol-induced chronic heart failure in rats].
abstract: OBJECTIVE
  To investigate the protective effects of oxymatrine on chronic heart failure induced by isoproterenol (ISO) and to observe its effects on ADMA metabolism pathway in ISO-induced chronic heart failure in rats.
  
  
  METHODS
  Male Sprague-Dawley rats were given oxymatrine (100,50 mg kg-1) orally for 14 days. Heart failure was induced in rats by subcutaneous injection of isoproterenol (5 mg kg-1 d-1 ) at the 8th day for 1 week. Serum parameters, haemodynamic parameters, Heart weight, and histopathological variables were analysed. Expression of protein levels were measured by Western blot.
  
  
  RESULTS
  Oxymatrine (100,50 mg kg-1) significantly attenuated serum content of cTn I, improved left ventricle systolic and diastolic function and left ventricular remodeling, reduced the ISO-induced myocardial pathological changes compared with ISO group. In addition, oxymatrine (100,50 mg kg-1) significantly reduced serum level of ADMA (P <0. 01), normalize the reduced dimethylarginine dimethylaminohydrolase 2 (DDAH2) expression (P <0. 01) , but had no effect on the isoproterenol-induced upregulated protein arginine methyltransferases 1 expression.
  
  
  CONCLUSIONS
  Oxymatrine could ameliorate the experimental ventricular remodeling in ISO-induced chronic heart failure in rats and the mechanism involved in reducing serum content of ADMA and increased DDAH2 expression.
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.forename: Ye-Hua
authors.initials: YH
authors.lastname: Xu
authors.forename: Ai-Qin
authors.initials: AQ
authors.lastname: Xiong
authors.forename: Ya-Ni
authors.initials: YN
authors.lastname: Yuan
authors.forename: Ping
authors.initials: P
authors.lastname: Zheng
authors.forename: Ping
authors.initials: P
authors.lastname: Ma
authors.forename: Gui-Dong
authors.initials: GD
authors.lastname: Dai
authors.forename: Qing-Bin
authors.initials: QB
authors.lastname: Xu
mesh_terms: D000470:Alkaloids / Q000494:pharmacology* / Q000627:therapeutic use; D000581:Amidohydrolases / Q000378:metabolism; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood / Q000378:metabolism; D002908:Chronic Disease; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D007545:Isoproterenol / Q000009:adverse effects*; D008297:Male; D009929:Organ Size / Q000187:drug effects; D011807:Quinolizines / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D019210:Troponin I / Q000378:metabolism; D000093842:Matrines
chemical_list: D000470:Alkaloids; D000581:Amidohydrolases; D001120:Arginine; D007545:Isoproterenol; D011807:Quinolizines; D019210:Troponin I; C487735:dimethylarginine; C037573:oxymatrine; D000093842:Matrines; C059999:dimethylargininase