Biomolecules & Therapeutics
The Effect of Galangin on the Regulation of Vascular Contractility via the Holoenzyme Reactivation Suppressing ROCK/CPI-17 rather than PKC/CPI-17
Hyuk-Jun Yoon1,†, Won Pill Jung1,†, Young Sil Min2, Fanxue Jin3, Joon Seok Bang4, Uy Dong Sohn5 and Hyun Dong Je1,*
1Department of Pharmacology, College of Pharmacy, Daegu Catholic University, Gyeongsan 38430,
2Department of Pharmaceutical Science, Jungwon University, Goesan 28024,
3Department of Pharmacology, Kyungpook National University School of Medicine, Daegu 41944,
4College of Pharmacy, Sookmyung Women’s University, Seoul 04310,
5Department of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Republic of Korea
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The first two authors contributed equally to this work.
Received: May 3, 2021; Revised: June 10, 2021; Accepted: June 18, 2021; Published online: July 7, 2021.
© The Korean Society of Applied Pharmacology. All rights reserved.

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In this study, we investigated the influence of galangin on vascular contractibility and to determine the mechanism underlying the relaxation. Isometric contractions of denuded aortic muscles were recorded and combined with western blot analysis which was performed to measure the phosphorylation of phosphorylation-dependent inhibitory protein of myosin phosphatase (CPI-17) and myosin phosphatase targeting subunit 1 (MYPT1) and to evaluate the effect of galangin on the RhoA/ROCK/CPI-17 pathway. Galangin significantly inhibited phorbol ester-, fluoride- and thromboxane mimetic-induced vasoconstrictions regardless of endothelial nitric oxide synthesis, suggesting its direct effect on vascular smooth muscle. Galangin significantly inhibited the fluoridedependent increase in pMYPT1 and pCPI-17 levels and phorbol 12,13-dibutyrate-dependent increase in pERK1/2 level, suggesting repression of ROCK and MEK activity and subsequent phosphorylation of MYPT1, CPI-17 and ERK1/2. Taken together, these results suggest that galangin-induced relaxation involves myosin phosphatase reactivation and calcium desensitization, which appears to be mediated by CPI-17 dephosphorylation via not PKC but ROCK inactivation.
Keywords: CPI-17, Fluoride, Galangin, MYPT1, Phorbol ester, ROCK

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