Protective effect of oxymatrine on chronic heart failure and ADMA metabolism pathway in isoproterenol-induced chronic heart failure in rats / 中国中药杂志
China Journal of Chinese Materia Medica
;
(24): 471-477, 2014.
Artículo
en Chino
| WPRIM
| ID: wpr-287563
ABSTRACT
<p><b>OBJECTIVE</b>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.</p><p><b>METHOD</b>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.</p><p><b>RESULT</b>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.</p><p><b>CONCLUSION</b>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.</p>
Texto completo:
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Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Tamaño de los Órganos
/
Patología
/
Farmacología
/
Arginina
/
Quinolizinas
/
Sangre
/
Regulación Enzimológica de la Expresión Génica
/
Enfermedad Crónica
/
Ratas Sprague-Dawley
/
Troponina I
Límite:
Animales
Idioma:
Chino
Revista:
China Journal of Chinese Materia Medica
Año:
2014
Tipo del documento:
Artículo
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