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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/33425
Title: Anti-angiogenic actions of the mangosteen polyphenolic xanthone derivative α-mangostin
Authors: Kanjana Jittiporn
Jutamas Suwanpradid
Chintan Patel
Modesto Rojas
Suwan Thirawarapan
Primchanien Moongkarndi
Wisuda Suvitayavat
Ruth B. Caldwell
Augusta University
Medical College of Georgia
Mahidol University
VA Medical Center
Keywords: Biochemistry, Genetics and Molecular Biology;Medicine
Issue Date: 1-Jan-2014
Citation: Microvascular Research. Vol.93, (2014), 72-79
Abstract: Retinal neovascularization is a major cause of vision loss in diseases characterized by retinal ischemia and is characterized by the pathological growth of abnormal vessels. Vascular endothelial growth factor (VEGF) is known to play an important role in this process. Oxidative stress has been strongly implicated in up-regulation of VEGF associated with neovascularization in various tissues. Hence, compounds with anti-oxidant actions can prevent neovascularization. α-Mangostin, a component of mangosteen (. Garcinia mangostana Linn), has been shown to have an anti-oxidant property in pathological conditions involving angiogenesis such as cancer. However, the effect of α-mangostin on ROS formation and angiogenic function in microvascular endothelial cells has not been studied. Hence, this study demonstrated the anti-angiogenic effects of α-mangostin in relation to ROS formation in bovine retinal endothelial cells (REC). α-Mangostin significantly and dose-dependently reduced formation of ROS in hypoxia-treated REC. α-Mangostin also significantly and dose-dependently suppressed VEGF-induced increases in permeability, proliferation, migration and tube formation in REC and blocked angiogenic sprouting in the ex vivo aortic ring assay. In addition, α-mangostin inhibited VEGF-induced phosphorylation of VEGFR2 and ERK1/2-MAPK. According to our results, α-mangostin reduces oxidative stress and limits VEGF-induced angiogenesis through a process involving abrogation of VEGFR2 and ERK1/2-MAPK activation. © 2014 Elsevier Inc.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84901236284&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/33425
ISSN: 10959319
00262862
Appears in Collections:Scopus 2011-2015

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