ArticleJournal of ginseng research2015
Inhibition of L-type Ca(2+) current by ginsenoside Rd in rat ventricular myocytes.
Article in Journal of ginseng research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Differential effects of ginsenosides on Ca2+ regulation in rotenone-treated neuronal and microglial cells.PloS one · 2026Article
- Natural L-type calcium channels antagonists from Chinese medicine.Chinese medicine · 2024Article
- The purified extract of steamedJournal of ginseng research · 2023Article
- Insights into Recent Studies on Biotransformation and Pharmacological Activities of Ginsenoside Rd.Biomolecules · 2022Review
- Ginseng extract and ginsenosides improve neurological function and promote antioxidant effects in rats with spinal cord injury: A meta-analysis and systematic review.Journal of ginseng research · 2022Review
- YiQiFuMai Powder Injection Attenuates Coronary Artery Ligation-Induced Heart Failure Through Improving Mitochondrial Function via Regulating ROS Generation and CaMKII Signaling Pathways.Frontiers in pharmacology · 2019Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGinsenoside Rd (GSRd), one of the most abundant ingredients of Panax ginseng, protects the heart via multiple mechanisms including the inhibition of Ca(2+) influx. We intended to explore the effects of GSRd on L-type Ca(2+) current (I Ca,L) and define the mechanism of the suppression of I Ca,L by GSRd.
methodsPerforated-patch recording and whole-cell voltage clamp techniques were applied in isolated rat ventricular myocytes.
results(1) GSRd reduced I Ca,L peak amplitude in a concentration-dependent manner [half-maximal inhibitory concentration (IC50) = 32.4 ± 7.1 μmol/L] and up-shifted the current-voltage (I-V) curve. (2) GSRd (30 μmol/L) significantly changed the steady-state activation curve of I Ca,L (V 0.5: -19.12 ± 0.68 vs. -16.26 ± 0.38 mV; n = 5, p < 0.05) and slowed down the recovery of I Ca,L from inactivation [the time content (ζ) from 91 ms to 136 ms, n = 5, p < 0.01]. (3) A more significant inhibitive effect of GSRd (100 μmol/L) was identified in perforated-patch recording when compared with whole-cell recording [65.7 ± 3.2% (n = 10) vs. 31.4 ± 5.2% (n = 5), p < 0.01]. (4) Pertussis toxin (G i protein inhibitor) completely abolished the I Ca,L inhibition induced by GSRd. There was a significant difference in inhibition potency between the two cyclic adenosine monophosphate elevating agents (isoprenaline and forskolin) prestimulation [55 ± 7.8% (n = 5) vs. 17.2 ± 3.5% (n = 5), p < 0.01]. (5) 1H-[1,2,4]Oxadiazolo[4,3-a]-quinoxalin-1-one (a guanylate cyclase inhibitor) and N-acetyl-l-cysteine (a nitric oxide scavenger) partly recovered the I Ca,L inhibition induced by GSRd. (6) Phorbol-12-myristate-13-acetate (a protein kinase C activator) and GF109203X (a protein kinase C inhibitor) did not contribute to the inhibition of GSRd.
conclusionThese findings suggest that GSRd could inhibit I Ca,L through pertussis toxin-sensitive G protein (Gi) and a nitric oxide-cyclic guanosine monophosphate-dependent mechanism.
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