Abstract
Objective: Sustained beta-adrenoceptor activation is deleterious to the heart due to induction of pathological remodeling and compromising cardiomyocytes viability that increase a risk for sudden cardiac death. Our and others studies suggest that melatonin and omega-3 fatty acids are cardioprotective but underlying mechanisms are not fully elucidated. We hypothesize that both compounds may affect extracellular matrix remodeling by modulation of MMPase activity. We aimed to investigate MMP-2 activity in plasma, aorta and heart of beta-agonist isoproterenol (iso) injured normotensive (Wistar) and hypertensive rats (SHR) in respect to omega-3 fatty acids (Omacor) and melatonin treatments. Design and method: Wistar and SHR were divided into four groups: controls without treatment; iso-injured rats (118 mg/kg totally, s.c., for 7 days); iso-injured rats treated with melatonin (10 mg/kg, p.o., 2 month); iso-injured rats treated with Omacor (1.68 g/kg, p.o., 2 month). MMP-2 activity was estimated using gelatin zymography. Results: There was higher plasma but lower heart tissue-related MMP-2 activity in non-treated SHR vs Wistar rats and no difference in aorta. Iso caused an increase of MMP-2 in plasma as well as atria and decrease in left as well as right ventricles of Wistar rats. In contrast, iso decreased MMP-2 in plasma, aorta and increased in left and right ventricles of SHR. Melatonin and Omacor suppressed plasma MMP-2 activity in iso-treated Wistar but not iso-SHR. Both compounds decreased MMP-2 activity in atria of iso-Wistar rats but increased in iso-SHR as well as decreased MMP-2 activity in the ventricles of iso-treated SHR only. Conclusions: These data indicates that both melatonin and Omacor modulate circulating and cardiovascular tissue-related MMP-2 activity and there are strain- and tissue-related differences.
Published Version
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