Effect of Kaempferol on Modulation of Vascular Contractility Mainly through PKC and CPI-17 Inactivation
10.4062/biomolther.2023.186
- Author:
Hyuk-Jun YOON
1
;
Heui Woong MOON
;
Young Sil MIN
;
Fanxue JIN
;
Joon Seok BANG
;
Uy Dong SOHN
;
Hyun Dong JE
Author Information
1. Department of Pharmacy, College of Pharmacy, Daegu Catholic University, Gyeongsan 38430, Republic of Korea
- Publication Type:Original Article
- From:Biomolecules & Therapeutics
2024;32(3):361-367
- CountryRepublic of Korea
- Language:EN
-
Abstract:
In this study, we investigated the efficacy of kaempferol (a flavonoid found in plants and plant-derived foods such as kale, beans, tea, spinach and broccoli) on vascular contractibility and aimed to clarify the detailed mechanism underlying the relaxation. Isometric contractions of divested muscles were stored and linked with western blot analysis which was carried out to estimate the phosphorylation of myosin phosphatase targeting subunit 1 (MYPT1) and phosphorylation-dependent inhibitory protein for myosin phosphatase (CPI-17) and to estimate the effect of kaempferol on the RhoA/ROCK/CPI-17 pathway. Kaempferol conspicuously impeded phorbol ester-, fluoride- and a thromboxane mimetic-derived contractions regardless of endothelial nitric oxide synthesis, indicating its direct effect on smooth muscles. It also conspicuously impeded the fluoride-derived elevation in phospho-MYPT1 rather than phospho-CPI-17 levels and phorbol 12,13-dibutyrate-derived increase in phospho-CPI-17 and phospho-ERK1/2 levels, suggesting the depression of PKC and MEK activities and subsequent phosphorylation of CPI-17 and ERK1/2. Taken together, these outcomes suggest that kaempferol-derived relaxation incorporates myosin phosphatase retrieval and calcium desensitization, which appear to be modulated by CPI-17 dephosphorylation mainly through PKC inactivation.
