دورية أكاديمية

Delphinidin and cyanidin inhibit PDGFAB-induced VEGF release in vascular smooth muscle cells by preventing activation of p38 MAPK and JNK.

التفاصيل البيبلوغرافية
العنوان: Delphinidin and cyanidin inhibit PDGFAB-induced VEGF release in vascular smooth muscle cells by preventing activation of p38 MAPK and JNK.
المؤلفون: Oak, M.-H., Bedoui, J. E., Madeira, S. V. F., Chalupsky, K., Schini-Kerth, V. B.
المصدر: British Journal of Pharmacology; Oct2006, Vol. 149 Issue 3, p283-290, 8p
مصطلحات موضوعية: POLYPHENOLS, VASCULAR endothelial growth factors, VASCULAR smooth muscle, BLOOD vessels, REACTIVE oxygen species, FLAVONOIDS
مستخلص: Background and purpose: Red wine polyphenols (RWPs) inhibit the expression of vascular endothelial growth factor (VEGF), a major pro-angiogenic and pro-atherosclerotic factor, in vascular smooth muscle cells (VSMCs). The aim of this study was to identify which red wine polyphenols were inhibitory and to determine the mechanism underlying the inhibitory effects. Experimental approach: Release of VEGF stimulated by platelet derived growth factorAB (PDGFAB), from human aortic VSMCs was measured by immunoassay and phosphorylation of kinases by Western blot analysis. The direct antioxidant properties of polyphenols were determined by electron paramagnetic resonance and the cellular formation of reactive oxygen species (ROS) by dichlorofluorescein. Key results: The inhibitory effect of RWPs on PDGFAB-induced release of VEGF was mimicked by delphinidin but not by quercetin, catechins, resveratrol, gallic acid or caffeic acid. In the anthocyanin class, not only delphinidin but also cyanidin prevented VEGF release whereas malvidin and peonidin were without effect. RWPs, delphinidin and cyanidin directly scavenged ROS and prevented the PDGFAB-induced formation of ROS in VSMCs. Malvidin and peonidin did not scavenge ROS but prevented the cellular formation of ROS. Although the p38 MAPK, ERK1/2 and JNK pathways have been involved in the PDGFAB-induced expression of VEGF, in our experiments, only phosphorylation of p38 MAPK and JNK was inhibited by RWPs, delphinidin and cyanidin. Conclusions and implications: Anthocyanins presenting a hydroxyl residue at position 3' are able to inhibit PDGFAB-induced VEGF expression by preventing activation of p38 MAPK and JNK in VSMCs. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Complementary Index
الوصف
تدمد:00071188
DOI:10.1038/sj.bjp.0706843