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Vascular Cell 2011
Insulin-Like Growth Factor-1 (IGF-1) Reduces ischemic changes and increases circulating angiogenic factors in experimentally - induced myocardial infarction in ratsAbstract: Adult male Sprague-Dawley rats were randomly divided into 10-days control, myocardial infarction, IGF-1 alone (2 μg/rat/day) and ISO+IGF-1 groups. Isoproterenol (ISO), a synthetic catecholamine was used to induce myocardial infarction. Serum transforming growth factor-β (TGF-β) and vascular endothelial growth factor (VEGF) levels were checked after 10-days of IGF-1 administration.There was a significant increase in heart weight after IGF-1 treatment. A significant increase in cardiac enzyme level (CK-MB and LDH) was seen in isoproterenol treated rats when compared to control group. IGF-1treatment induced a significant increase in serum angiogenic factors, IGF-1, VEGF and TGF beta levels. IGF-1 also reduced the ischemic changes in the myocardium when compared to the isoproterenol alone treated group.In conclusion, treatment with insulin-like growth factor-1 (IGF-1) in myocardial infarction significantly increased circulating angiogenic growth factors like IGF-1, VEGF and TGF beta thus, protecting against myocardial ischemia.Cardiovascular disease is the leading cause of mortality, not only in the Western world, but also in developing countries [1]. Coronary artery disease is a global health concern today, with limited treatment options available to address this disorder. Extensive efforts have been devoted to molecular therapies to enhance perfusion and function of the ischemic myocardium [2]. Angiogenesis is a process involving the formation of new blood vessels from the pre-existing vasculature that occurs in many physiological and pathological situations [3]. Although neovascularization is an important vascular response to chronic hypoxia, the role of angiogenesis in myocardial ischemia remains unclear [4,5]. Therapeutic angiogenesis is being tested as a novel treatment for ischemic heart disease [2]. In this connection, the challenge in the last decennium has been to find methods of inducing new vascular growth in the ischemic myocardium of patients suffering fro
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