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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2010) 34, S33 (Printed in Great Britain)
Meeting Abstract
Calcitonin gene-related peptide-mediated protective effect of rutaecarpine against endothelial cell injury induced by lysopbosphatidylcholine
Dan Luo1, Wei Jie Peng2 and Hong Xu1
1Department of Physiology, Medical College of Nanchang University, Nanchang, and 2Department of Pharmacology, Medical College of Nanchang University, Nanchang, China


It has been shown that the cadioprotection of rutaecarpine is mediated by calcitonin gene-related peptide (CGRP) via activation of vanilloid receptor subtype 1 (VR1). Vascular endothelial cells can also synthesize CGRP and CGRP could protect against endothelial dysfunction induced by lysopbosphatidylcholine (LPC). In the present study, we explored whether the endothelial cell-derived CGRP is involved in the protective effect of rutaecarpine against endothelial cell damages. Human umbilical vein endothelial cells (HUVECs) were treated with rutaecarpine (10-7, 3 × 10-7 or 10-6 M) for 24 h. Endothelial cell injury was induced by LPC (5 mg/l), and evaluated by cell viability and lactate dehydrogenase activity. The level of CGRP mRNA was detected by RT-PCR, and protein level was measured by radioimmunoassay. Treatment with rutaecarpine increased the production of endothelium-derived CGRP in a concentration-dependent manner, which was abolished by capsazepine, a competitive antagonist of VR1. Rutaecarpine significantly attenuated the endothelial cell damage induced by LPC, which was prevented and aggravated by capsazepine or CGRP (8-37), antagonist of CGRP receptor. The present results suggest that rutaecarpine prevent LPC-induced endothelial injury, which is related to upregulation the expression of CGRP via activation of VR1 in endothelial cells.




Published online 1 August 2010, doi:10.1042/CBI034S033a


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ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)