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The effect of calcium channel blockade on matrix metalloproteinases and fibronectin in the rat myocardial remodeling / 中国药理学通报
Chinese Pharmacological Bulletin ; (12)2003.
Artigo em Chinês | WPRIM | ID: wpr-559721
ABSTRACT
Aim To investigate the contribution of cardiac L-and L/T-type Ca 2+ channels blockers on matrix metalloproteinases (MMPs) protein expression and fibronectin (FN) degradation following myocardial infarction(MI). Methods Rat MI model was established by permanent ligation of left coronary artery. Infarcted rats were orally treated with placebo, amlodipine (L-channel blocker, 4 mg?kg -1?d -1) or mibefradil (L/T-Channel blocker, 10 mg?kg -1?d -1) for 7 days before induction of myocardial infarction. Protein levels of MMP-2,3,9 and FN distribution were assayed by immunoflorescence at 1, 3, 7 days post coronary occlusion in left ventricular free wall (LVFW) and myocardium interventricular septum (IS). Results Pathological changes of myocardial tissues in IS and LVFW showed typical myocardial remodeling. The hypertrophy was dominant in IS, but in LVFW the characteristics including disordered alignament, hypertrophy of the myocytes, the discontinuity, dissolving of carediomyofibrills, and the hyperplasia of interstitial tissue were found 7 days after MI. The protein levels of MMP-2,3,9 increased in IS 1,3,7 days post MI gradually, whereas the protein levels of FN decreased gradually, the protein levels of MMP-2,3,9 increased significantly in LVFW 7 days post MI, and the protein levels of FN decreased significantly compared to control group, respectively(P

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Tipo de estudo: Ensaio Clínico Controlado / Estudo prognóstico Idioma: Chinês Revista: Chinese Pharmacological Bulletin Ano de publicação: 2003 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Tipo de estudo: Ensaio Clínico Controlado / Estudo prognóstico Idioma: Chinês Revista: Chinese Pharmacological Bulletin Ano de publicação: 2003 Tipo de documento: Artigo