Resveratrol ameliorates myocardial damage by inducing vascular endothelial growth factor-angiogenesis and tyrosine kinase receptor Flk-1

• Published in: Cell biochemistry and biophysics Vol. 44; no. 1; pp. 43 - 50
• Main Authors: Fukuda, Shoji, Kaga, Shigeaki, Zhan, Lijun, Bagchi, Debasis, Das, Dipak K, Bertelli, Aldo, Maulik, Nilanjana
• Format: Journal Article
• Language: English
• Published: United States Springer Nature B.V 2006
• Subjects: Angiogenesis Inducing Agents - pharmacology; Animals; Anti-Inflammatory Agents, Non-Steroidal - pharmacology; Apoptosis; DNA - metabolism; Heart - drug effects; Heart attacks; Heart Function Tests; Male; Microcirculation - drug effects; Molecular Structure; Myocardial infarction; Myocardial Infarction - drug therapy; Myocardial Infarction - pathology; Myocardium - metabolism; Myocardium - pathology; Neovascularization, Physiologic - drug effects; NF-kappa B - metabolism; Nitric Oxide Synthase Type II - metabolism; Nitric Oxide Synthase Type III - metabolism; Protein Binding - drug effects; Proteins; Rats; Rats, Sprague-Dawley; Rodents; Sp1 Transcription Factor - metabolism; Stilbenes - pharmacology; Vascular Endothelial Growth Factor A - metabolism; Vascular Endothelial Growth Factor Receptor-2 - metabolism; Ventricular Function, Left - drug effects
• ISSN: 1085-9195; 1085-9195; 1559-0283
• DOI: 10.1385/cbb:44:1:043

In our study, resveratrol (polyphenol) has been identified as a very important stimulus/agent for the induction of new vessel growth. Occlusion of a main coronary depletes the blood supply to the myocardium and subsequently reduces cardiac function, which ultimately leads to heart failure. Progressive, chronic coronary artery occlusion has been shown to induce development of collateral arteries to re-establish and maintain blood flow to the myocardium at risk via the growth of new capillary vessels or angiogenesis. Studies from our laboratory, as well as from others, have already confirmed the protective role of collaterals against myocardial ischemia and cell death. We have successfully demonstrated in rat myocardial infarction (MI) model an effect of resveratrol on significant upregulation of the protein expression profiles of vascular endothelial growth factor (VEGF) and its tyrosine kinase receptor Flk-1, 3 wk after MI. Pretreatment with resveratrol also increased nitric-oxide synthase (inducible NOS and endothelial NOS) along with increased antiapoptotic and proangiogenic factors nuclear factor (NF)-kappaB and specificity protein (SP)-1. We also were able to demonstrate increased capillary density as well as improved left ventricular function by pharmacological preconditioning with resveratrol 3 wk after MI.