ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2012
Ginsenoside-Rd attenuates TRPM7 and ASIC1a but promotes ASIC2a expression in rats after focal cerebral ischemia.
Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Neuroprotective Effect and Possible Mechanisms of Ginsenoside-Rd for Cerebral Ischemia/Reperfusion Damage in Experimental Animal: A Meta-Analysis and Systematic Review.Oxidative medicine and cellular longevity · 2022Pooled it
- Ginsenoside Rd Is Efficacious Against Acute Ischemic Stroke by Suppressing Microglial Proteasome-Mediated Inflammation.Molecular neurobiology · 2016Trial
- Hypoxia and interleukin-1-primed mesenchymal stem/stromal cells as novel therapy for stroke.Human cell · 2024Review
- Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7.Frontiers in cell and developmental biology · 2023Review
- Biotransformation, Pharmacokinetics, and Pharmacological Activities of Ginsenoside Rd Against Multiple Diseases.Frontiers in pharmacology · 2022Review
- A Review of Neuroprotective Effects and Mechanisms of Ginsenosides From Panax Ginseng in Treating Ischemic Stroke.Frontiers in pharmacology · 2022Review
- Neuroprotective Phytochemicals in Experimental Ischemic Stroke: Mechanisms and Potential Clinical Applications.Oxidative medicine and cellular longevity · 2021Review
- Mapping TRPM7 Function by NS8593.International journal of molecular sciences · 2020Review
- Article
- Factors and Molecular Mechanisms Influencing the Protein Synthesis, Degradation and Membrane Trafficking of ASIC1a.Frontiers in cell and developmental biology · 2020Review
- Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF-β1/Smads signaling pathway by targeting TRPM6.Cell cycle (Georgetown, Tex.) · 2019Article
- Efficacy and Mechanism of Panax Ginseng in Experimental Stroke.Frontiers in neuroscience · 2019Review
- Beneficial effects ofJournal of ginseng research · 2018Review
- Ginsenoside Reduces Cognitive Impairment During Chronic Cerebral Hypoperfusion Through Brain-Derived Neurotrophic Factor Regulated by Epigenetic Modulation.Molecular neurobiology · 2017Article
- Acid-Sensing Ion Channels as Potential Therapeutic Targets in Neurodegeneration and Neuroinflammation.Mediators of inflammation · 2017Review
- A Role of Ginseng and Its Constituents in the Treatment of Central Nervous System Disorders.Evidence-based complementary and alternative medicine : eCAM · 2016Review
- Ginsenoside Rd and ischemic stroke; a short review of literatures.Journal of ginseng research · 2015Review
- TRPM7 inhibitor carvacrol protects brain from neonatal hypoxic-ischemic injury.Molecular brain · 2015Article
- Protective effects of ginseng on neurological disorders.Frontiers in aging neuroscience · 2015Review
- Acid-sensing ion channels: potential therapeutic targets for neurologic diseases.Translational neurodegeneration · 2015Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous studies have showed that ginsenoside (GS)-Rd, a mono-compound isolated from traditional Chinese herb panax ginseng, has the neuroprotective effects following ischemic stroke. However, the underlying mechanisms are still largely unknown. Our latest study showed that GS-Rd could block calcium influx in cultured cortical neurons after excitotoxic injury, indicating that GS-Rd may act on cation channels. To explore this possibility, in this study, we used a rat middle cerebral artery occlusion (MCAO) model to examine the effects of GS-Rd on the expression of non-selective cation channels, including transient receptor potential melastatin (TRPM) and acid sensing ion channels (ASIC), and cation channels, including N-methyl-D-aspartate (NMDA) receptors, which all play essential roles in ischemic stroke. Our results showed that both TRPM and ASIC channels were expressed in the brain. At 24 h following MCAO insult, mRNA and protein expression levels of TRPM7, ASIC1a and ASIC2a were significantly increased. Pretreatment of 10 mg/kg GS-Rd attenuated MCAO-induced expression of TRPM7 and ASIC1a but promoted that of ASIC2a. In contrast, GS-Rd had no significant effects on the expression of NMDA receptors. Thus, our results suggest that GS-Rd neuroprotection following cerebral ischemia may be at least due to its effects on the expression of TRPM7, ASIC1a and ASIC2a.
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