ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Cardiovascular and Smooth Muscle Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1573483
This article is part of the Research TopicInnovative Approaches and Molecular Mechanisms in Cardiovascular PharmacologyView all 10 articles
Trifolin inhibits the calcium-driven contraction pathway in vascular smooth muscle
Provisionally accepted
- Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian Province, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Trifolin, a bioactive component of the Qingda granule, has demonstrated significant antihypertensive potential; however, its precise mechanisms of action remain largely unknown. This study aimed to investigate the antihypertensive effects of trifolin and unravel its underlying molecular mechanisms. The influence of trifolin on vascular contraction and relaxation and its regulatory effects on ion channels were evaluated through a vascular tension experiment. Morphological changes in the aortic tissues of mice with angiotensin Ⅱ-induced hypertension and the expression profiles of contraction-associated proteins were analyzed via hematoxylin-eosin staining and immunohistochemistry. Additionally, trifolin's impact on calcium ion dynamics and contraction-associated protein expression in angiotensin Ⅱ-activated vascular smooth muscle cells (VSMCs) was determined through calcium flux assays and western blot analyses. Trifolin treatment decreased the constriction of isolated abdominal aortic rings induced by norepinephrine, KCl, and angiotensin Ⅱ in an endotheliumindependent manner and extracellular Ca 2 ⁺ influx induced by these three substances and thapsigargin. Moreover, trifolin treatment significantly reduced the abdominal aortic wall thickness and downregulated the expression of store-operated channels channel proteins (STIM1 and ORAI1) and calcium signaling-related proteins (CaM, myosin light chain kinase, and p-MLC2) in the abdominal aorta of hypertensive mice and angiotensin Ⅱ-induced VSMCs. In conclusion, calcium signaling inhibition may underlie trifolin's antihypertensive effects and its ability to ameliorate vascular function.These findings offer new therapeutic insights for hypertension treatment.
Keywords: trifolin, Hypertension, Vasoconstriction, Calcium signaling pathway, Smooth vascular muscle
Received: 09 Feb 2025; Accepted: 16 May 2025.
Copyright: © 2025 Li, Wu, Wu, Ali, Yang, Chen, Guo, Lian, Shen and Peng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Dawei Lian, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian Province, China
Aling Shen, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian Province, China
Jun Peng, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian Province, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.