Corosolic Acid Induces Endothelium-Dependent Vasorelaxation in Isolated Rat Aortic Rings.
F, C., WY, T., MT, O., & MF, Y. (2026). Corosolic Acid Induces Endothelium-Dependent Vasorelaxation in Isolated Rat Aortic Rings.. Molecules (Basel, Switzerland). https://doi.org/10.3390/molecules31162822
F C, WY T, MT O, MF Y. Corosolic Acid Induces Endothelium-Dependent Vasorelaxation in Isolated Rat Aortic Rings.. Molecules (Basel, Switzerland). 2026; doi: 10.3390/molecules31162822
F C, WY T, MT O, et al. Corosolic Acid Induces Endothelium-Dependent Vasorelaxation in Isolated Rat Aortic Rings.[J]. Molecules (Basel, Switzerland). 2026. DOI: 10.3390/molecules31162822.
@article{f2026,
author = {Chen F and Tew WY and Ong MT and Yam MF},
title = {Corosolic Acid Induces Endothelium-Dependent Vasorelaxation in Isolated Rat Aortic Rings.},
journal = {Molecules (Basel, Switzerland)},
year = {2026},
doi = {10.3390/molecules31162822},
note = {PMID: 42653903},
}
TY - JOUR AU - Chen F AU - Tew WY AU - Ong MT AU - Yam MF TI - Corosolic Acid Induces Endothelium-Dependent Vasorelaxation in Isolated Rat Aortic Rings. T2 - Molecules (Basel, Switzerland) PY - 2026 DO - 10.3390/molecules31162822 AN - PMID:42653903 ER -
The effect of Corosolic acid (CA) on vascular tone and the possible mecha-nisms involved remain unclear. The SPF-grade male Sprague-Dawley rats (Animal Ethics Approval ID: USM/IACUC/2025/(155)(1406)) were used. The vasorelaxant effects of CA were evaluated in endothelium-intact and endothelium-denuded rings precontracted with phenylephrine (PE), and in endothelium-intact rings precontracted with KCl. Possible mechanisms were examined using L-NAME, ODQ, methylene blue, indomethacin, atropine, propranolol, and potassium channel blockers (glibenclamide, TEA, BaCl2, and 4-AP). The effects of CA on voltage-operated calcium channels (VOCCs) and IP3 receptor (IP3R)-mediated sarcoplasmic reticulum calcium release were also assessed. CA concentration-dependently relaxed endothelium-intact aortic rings precontracted with PE (RMAX = 90.08 ± 7.33%; pD2 = 4.21 ± 0.08). The relaxation response was markedly reduced after endothelial removal and in KCl-precontracted rings. EDRF pathway inhibitors (L-NAME, ODQ, methylene blue, and indomethacin) and GPCR-related antagonists (atropine and propranolol) attenuated CA-induced relaxation. Among potassium channel blockers, glibenclamide and TEA showed stronger inhibitory effects. CA did not significantly inhibit VOCC-mediated CaCl2-induced contraction but partially reduced PE-induced contraction under calcium-free conditions. The mechanisms for CA treating hypertension may involve NO/cGMP signalling, COX-related prostanoid pathways, GPCR-related mechanisms, potassium channel modulation, and partial inhibition of IP3R-mediated calcium release.