Mechanistic Studies of AVE3085 Against Homocysteine in Endothelial Protection
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ORIGINAL ARTICLE
Mechanistic Studies of AVE3085 Against Homocysteine in Endothelial Protection Qin Yang & Hong-Mei Xue & Malcolm John Underwood & Cheuk-Man Yu
# Springer Science+Business Media New York 2013
Abstract Purpose Homocysteine (Hcy) is an independent risk factor for cardiovascular diseases that impairs endothelial function. We investigated whether the impaired endothelial function can be restored by the eNOS transcription enhancer AVE3085 in porcine coronary arteries. The effects of AVE3085 against Hcy on eNOS-NO function were studied and further investigations were conducted to reveal the role of arginase and the signaling pathway of eNOS activation in the effect of AVE3085 on endothelial dysfunction caused by Hcy. Methods Myograph study of vasorelaxation, electrochemical measurement of NO, RT-PCR and Western blot analysis of eNOS, iNOS expression, and eNOS phosphorylation were performed. Arginase activity was determined by urea production and O2.− generation by lucigenin-enhanced chemiluminenscence. Qin Yang and Hong-Mei Xue contribute equally. Electronic supplementary material The online version of this article (doi:10.1007/s10557-013-6478-5) contains supplementary material, which is available to authorized users. Q. Yang (*) Division of Cardiology, Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong & TEDA International Cardiovascular Hospital, Medical College, Nankai University, Tianjin, China e-mail: [email protected] H.
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