Protective effect of oxymatrine on chronic heart failure and ADMA metabolism pathway in isoproterenol-induced chronic heart failure in rats.
- Author:
Yang WANG
;
Ye-Hua XU
;
Ai-Qin XIONG
;
Ya-Ni YUAN
;
Ping ZHENG
;
Ping MA
;
Gui-Dong DAI
;
Qing-Bin XU
- Publication Type:Journal Article
- MeSH: Alkaloids; pharmacology; therapeutic use; Amidohydrolases; metabolism; Animals; Arginine; analogs & derivatives; blood; metabolism; Chronic Disease; Gene Expression Regulation, Enzymologic; drug effects; Heart Failure; drug therapy; metabolism; pathology; physiopathology; Hemodynamics; drug effects; Isoproterenol; adverse effects; Male; Organ Size; drug effects; Quinolizines; pharmacology; therapeutic use; Rats; Rats, Sprague-Dawley; Troponin I; metabolism
- From: China Journal of Chinese Materia Medica 2014;39(3):471-477
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo 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.
METHODMale 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.
RESULTOxymatrine (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.
CONCLUSIONOxymatrine 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.