Allicin Inhibits Blood Vessel Growth and Downregulates Akt Phosphorylation and Actin Polymerization

2008 
INTRODUCTION Angiogenesis is a multistep cellular process in which new vessels emerge from preexisting endothelial vasculature in the presence of various growth factors and extracellular matrix (ECM) proteins (1). This process includes movement of endothelial cells (EC) to the site of future vessel development, proliferation, and formation of tubule-like structures followed by recruitment of pericytes and smooth muscle cells, that is, vessel maturation (1). Evidently, initial stages of vessel growth are dependent on the integrity of cellular cytoskeleton in ECs and the ability of intracellular monomeric actin to polymerize (2). Angiogenesis underlies a wide spectrum of both physiologic and pathologic processes including primary tumor growth, invasion, and metastases (3,4). In addition, inflammation and angiogenesis are linked together (5), and blood vessel growth constitutes an essential part in the pathogenesis of a number of inflammatory-mediated diseases including inflammatory bowel disease and rheumatoid arthritis (6,7). Therefore, inhibition of angiogenesis is a challenge that modern biology faces, and the development of novel antiangiogenic agents is highly important. Allicin (diallyl-thiosulfinate) is a major ingredient of fresh garlic extract. It is produced during the crushing of garlic cloves
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