BMC complementary medicine and therapies · 2026
Bilobalide increases SKCa current via 5-HT2BR-PLC-PKC pathway, causing hyperpolarization and enhanced EET production in human coronary artery endothelial cells.
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Ruamyod Katesirin, Taokum Patcharaporn, Wongsatan Neennara, Tapechum Sompol, Watanapa Wattana B
Аннотация
BACKGROUND: Ginkgo biloba extract and its active component bilobalide induce endothelium-dependent vasodilation in coronary and other vascular beds. This effect is associated with increased Ca2+-activated K+ channel activity in endothelial cells. We aimed to identify ion channels targeted by bilobalide in human coronary artery endothelial cells (HCAECs) and to explore the underlying mechanisms.
METHODS: Whole-cell patch-clamp recordings were performed on cultured HCAECs. Epoxyeicosatrienoic acids (EETs) and prostacyclin were quantified with enzyme-linked immunosorbent assays; nitric oxide and hydrogen peroxide were assessed with commercial kits.
RESULTS: Bilobalide dose-dependently increased whole-cell current through activation of the small-conductance Ca2+-activated K+ (SKCa) channel, but not through Cl-, transient receptor potential, or other K+ channels. The current increase persisted when all channels except SKCa were blocked and was abolished by apamin, a selective SKCa blocker; additionally, apamin prevented bilobalide-stimulated current. Bilobalide also induced HCAEC hyperpolarization, which was inhibited by apamin. The bilobalide-induced current increase was blocked by antagonists of 5-hydroxytryptamine (5-HT)1/2 and 5-HT2B receptors, phospholipase C, and protein kinase C, but not by inhibitors of 5-HT1B receptors, cytochrome P450, or Gi/o proteins. Furthermore, bilobalide stimulated EET production but not nitric oxide, prostacyclin, or hydrogen peroxide production; this effect was also apamin-sensitive.
CONCLUSIONS: Bilobalide increases HCAEC current and induces hyperpolarization by activating SKCa via the 5-HT2B receptor-phospholipase C-protein kinase C signaling pathway, leading to EET generation. These findings provide insights into bilobalide's endothelial mechanisms and highlight its potential as an alternative therapy for coronary artery disease.
METHODS: Whole-cell patch-clamp recordings were performed on cultured HCAECs. Epoxyeicosatrienoic acids (EETs) and prostacyclin were quantified with enzyme-linked immunosorbent assays; nitric oxide and hydrogen peroxide were assessed with commercial kits.
RESULTS: Bilobalide dose-dependently increased whole-cell current through activation of the small-conductance Ca2+-activated K+ (SKCa) channel, but not through Cl-, transient receptor potential, or other K+ channels. The current increase persisted when all channels except SKCa were blocked and was abolished by apamin, a selective SKCa blocker; additionally, apamin prevented bilobalide-stimulated current. Bilobalide also induced HCAEC hyperpolarization, which was inhibited by apamin. The bilobalide-induced current increase was blocked by antagonists of 5-hydroxytryptamine (5-HT)1/2 and 5-HT2B receptors, phospholipase C, and protein kinase C, but not by inhibitors of 5-HT1B receptors, cytochrome P450, or Gi/o proteins. Furthermore, bilobalide stimulated EET production but not nitric oxide, prostacyclin, or hydrogen peroxide production; this effect was also apamin-sensitive.
CONCLUSIONS: Bilobalide increases HCAEC current and induces hyperpolarization by activating SKCa via the 5-HT2B receptor-phospholipase C-protein kinase C signaling pathway, leading to EET generation. These findings provide insights into bilobalide's endothelial mechanisms and highlight its potential as an alternative therapy for coronary artery disease.