pISSN 1226-4512 eISSN 2093-3827


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Original Article

Korean J Physiol Pharmacol 2013; 17(1): 31-36

Published online February 28, 2013 https://doi.org/10.4196/kjpp.2013.17.1.31

Copyright © The Korean Journal of Physiology & Pharmacology.

The Inhibitory Effect of Eupatilin on the Agonist-Induced Regulation of Vascular Contractility

Hyun Dong Je1,*, Hyeong-Dong Kim2,*, and Ji Hoon Jeong3,4

1Department of Pharmacology, College of Pharmacy, Catholic University of Daegu, Gyeongbuk 712-702, 2Department of Physical Therapy, College of Health Science, Korea University, Seoul 136-701, 3Department of Pharmacology, College of Medicine, Chung-Ang University, 4Research Institute for Translational System Biomics, Chung-Ang University, Seoul 156-756, Korea

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


The present study was undertaken to investigate the influence of eupatilin on vascular smooth muscle contractility and to determine the mechanism involved. Denuded aortic rings from male rats were used and isometric contractions were recorded and combined with molecular experiments. Eupatilin more significantly relaxed fluoride-induced vascular contraction than thromboxane A2 or phorbol ester-induced contraction suggesting as a possible anti-hypertensive on the agonist-induced vascular contraction regardless of endothelial nitric oxide synthesis. Furthermore, eupatilin significantly inhibited fluoride-induced increases in pMYPT1 levels. On the other hand, it didn't significantly inhibit phorbol ester-induced increases in pERK1/2 levels suggesting the mechanism involving the primarily inhibition of Rho-kinase activity and the subsequent phosphorylation of MYPT1. This study provides evidence regarding the mechanism underlying the relaxation effect of eupatilin on agonist- induced vascular contraction regardless of endothelial function.

Keywords: ERK1/2, Eupatilin, MYPT1, Rho-kinase, Vasodilation