Work

Cinnamaldehyde prevents coronary artery spasm by down-regulating the function and expression of voltage-gated Ca2+ channels and Ca2+ -activated Cl- channels in the arterial smooth muscle cells

Year: 2025

Type: article

Abstract: Background Cinnamaldehyde (CinA) is a phytochemical whose source plants are widely used as a medicine and food spice additive, but its vascular effect and mechanisms remain poorly understood. Purpose To study the vasomotor effect and channel pharmacological effect of CinA on the arterial smooth muscle cells (ASMC) of rat coronary artery (RCA). Methods The tensions of rat isolated arteries were recorded with a myograph. Transmembrane currents through Ca 2+ -activated Cl - channels (CaCC), voltage-gated K + (Kv) channels and inwardly rectifier K + (Kir) channels were evaluated with a whole cell patch clamp. Intracellular Ca 2+ ([Ca 2+ ] i ) levels were measured with fluorescent dye Fluo-4 AM. Ion channel expressions were assayed with immunofluorescent staining and RT-qPCR. Results CinA relaxed all arteries tested. Among arteries contracted with various vasoconstrictors, 60 mM KCl-precontracted RCAs were more sensitive to the relaxation. Both intracellular Cl - depletion and CaCC inhibitor T16A inh -A01 decreased, while Kv inhibitor 4-aminopyridine increased, CinA-induced relaxation in serotonin-precontracted RCA. In RCA ASMC, CinA suppressed KCl-induced [Ca 2+ ] i elevation and decreased currents through CaCC, Kv channels and Kir channels. CinA incubation depressed the contractility of RCA and reduced expressions of VGCC, CaCC, Kv channels and Kir channels in RCA ASMC. Conclusion CinA induces vasorelaxation in various arteries and its vasorelaxation efficiencies vary with arteries and vasoconstrictors. Down-regulation of VGCC and CaCC contributes to the coronarospasmolysis of CinA, while repression on Kv channels and Kir channels may slightly discount the coronarospasmolysis. Overall, CinA may be a promising candidate to treat or prevent coronarospasmodic diseases.

Source: Biomedicine & Pharmacotherapy

DOI: 10.1016/j.biopha.2025.118213