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Effect of hydrogen sulfide donor on oxidative stress of myocardium in adriamycin-induced dilated cardiomyopathy rats / 中国病理生理杂志
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-530948
Biblioteca responsável: WPRO
ABSTRACT

AIM:

To investigate the effect of hydrogen sulfide(H2S)donor(NAHS)on oxidative stress of adriamycin-induced dilated cardiomyopathy rats.

METHODS:

Weight-matched adult male Wistar rats were randomly divided into 5 groups as follows(1)ADR group(n=12),in which 2.5 mg/kg of adriamycin was injected intraperitoneally once a week for 10 weeks(total dose of 25 mg/kg).(2)ADR+small-dose NaHS group(n=12),in which the dosage and the use of adriamycin were as mentioned above,while NaHS solution was injected to rats at a dosage of 2.8 ?mol?kg-1?d-1 at the same time.(3)ADR + large-dose NaHS group(n=12),in which the dosage and the use of adriamycin were as mentioned above,while NaHS solution was injected to rats at a dosage of 14 ?mol?kg-1?d-1 at the same time.(4)Control group(n=9),in which an equivalent volume of physiological saline was administered weekly for a total of 10 weeks.(5)NaHS group(n=9),in which 14 ?mol/kg of NaHS solution was injected to rats intraperitonealy once a week for 10 weeks.Hemodynamic and echocardiographic measurements were obtained 10 weeks after the treatment.Meanwhile,H2S and malondialdehyde(MDA)concentrations,the activities of superoxide dismutase(SOD)and glutathione peroxidase(GSH-Px)in serum and myocardial tissues were evaluated,respectively.

RESULTS:

The cardiac functions in the group of ADR rats depressed obviously.H2S concentrations,SOD and GSH-Px activities in serum and myocardial tissues of ADR group rats were all significantly decreased as compared with those in the control group(P

Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 2000 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pathophysiology Ano de publicação: 2000 Tipo de documento: Artigo
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