Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
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.
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Yang Xiaomin, Xu Xiaojia, Liu Yu, Wang Yan, Hou Xiaomin, Cao Jing, Zhang Mingsheng
Аннотация
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 Ca2+-activated Cl- channels (CaCC), voltage-gated K+ (Kv) channels and inwardly rectifier K+ (Kir) channels were evaluated with a whole cell patch clamp. Intracellular Ca2+ ([Ca2+]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 T16Ainh-A01 decreased, while Kv inhibitor 4-aminopyridine increased, CinA-induced relaxation in serotonin-precontracted RCA. In RCA ASMC, CinA suppressed KCl-induced [Ca2+]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.
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 Ca2+-activated Cl- channels (CaCC), voltage-gated K+ (Kv) channels and inwardly rectifier K+ (Kir) channels were evaluated with a whole cell patch clamp. Intracellular Ca2+ ([Ca2+]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 T16Ainh-A01 decreased, while Kv inhibitor 4-aminopyridine increased, CinA-induced relaxation in serotonin-precontracted RCA. In RCA ASMC, CinA suppressed KCl-induced [Ca2+]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.