ArticleMolecules and cells2011
Ginsenoside Rg3 enhances large conductance Ca2+-activated potassium channel currents: a role of Tyr360 residue.
Article in Molecules and cells, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Botanical drugs for treating erectile dysfunction: clinical evidence.Frontiers in pharmacology · 2023Review
- Emerging signals modulating potential of ginseng and its active compounds focusing on neurodegenerative diseases.Journal of ginseng research · 2019Review
- Molecular Basis of Altered hERG1 Channel Gating Induced by Ginsenoside Rg3.Molecular pharmacology · 2017Article
- Ginsenoside Rg3, a Gating Modifier of EAG Family K+ Channels.Molecular pharmacology · 2016Article
- Ginseng gintonin activates the human cardiac delayed rectifier K+ channel: involvement of Ca2+/calmodulin binding sites.Molecules and cells · 2014Article
- Relationships between chemical structures and functions of triterpene glycosides isolated from sea cucumbers.Frontiers in chemistry · 2014Review
- Ginseng ginsenoside pharmacology in the nervous system: involvement in the regulation of ion channels and receptors.Frontiers in physiology · 2014Review
- Yin and Yang of ginseng pharmacology: ginsenosides vs gintonin.Acta pharmacologica Sinica · 2013Review
- A comprehensive review of the therapeutic and pharmacological effects of ginseng and ginsenosides in central nervous system.Journal of ginseng research · 2013Article
- Molecular mechanisms of large-conductance ca (2+) -activated potassium channel activation by ginseng gintonin.Evidence-based complementary and alternative medicine : eCAM · 2013Article
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Authors and funding
9 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Ginsenosides, active ingredients of Panax ginseng, are known to exhibit neuroprotective effects. Large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels are key modulators of cellular excitability of neurons and vascular smooth muscle cells. In the present study, we examined the effects of ginsenosides on rat brain BK(Ca) (rSlo) channel activity heterologously expressed in Xenopus oocytes to elucidate the molecular mechanisms how ginsenoside regulates the BK(Ca) channel activity. Ginsenoside Rg(3) (Rg(3)) enhanced outward BK(Ca) channel currents. The Rg(3)-enhancement of outward BK(Ca) channel currents was concentration-dependent, voltage-dependent, and reversible. The EC(50) was 15.1 ± 3.1 μM. Rg(3) actions were not desensitized by repeated treatment. Tetraetylammonium (TEA), a K(+) channel blocker, inhibited BK(Ca) channel currents. We examined whether extracellular TEA treatment could alter the Rg(3) action and vice versa. TEA caused a rightward shift of the Rg(3) concentration-response curve (i.e., much higher concentration of Rg(3) is required for the activation of BK(Ca) channel compared to the absence of TEA), while Rg(3) caused a rightward shift of the TEA concentration-response curve in wild-type channels. Mutation of the extracellular TEA binding site Y360 to Y360I caused a rightward shift of the TEA concentration-response curve and almost abolished both the Rg(3) action and Rg(3)-induced rightward shift of TEA concentration-response curve. These results indicate that Tyr360 residue of BK(Ca) channel plays an important role in the Rg(3)-enhancement of BK(Ca) channel currents.
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