ArticleCellular and molecular neurobiology2016
Involvement of Connexin40 in the Protective Effects of Ginsenoside Rb1 Against Traumatic Brain Injury.
Article in Cellular and molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- The Dual Role of Connexins in Stroke, Neurotrauma, Neurodegenerative and Psychiatric Disorders: A Global Systematic Review.Molecules (Basel, Switzerland) · 2026Pooled it
- Gasotransmitters in the regulation of connexins in central and peripheral nervous system injuries.Medical gas research · 2027Review
- Progress of Ginsenoside Rb1 in neurological disorders.Frontiers in pharmacology · 2024Review
- Therapy of traumatic brain injury by modern agents and traditional Chinese medicine.Chinese medicine · 2023Review
- Involvement of Autophagy in the Protective Effects of Ginsenoside Rb1 in a Rat Model of Traumatic Brain Injury.European journal of drug metabolism and pharmacokinetics · 2022Article
- Article
- GAP junctions: multifaceted regulators of neuronal differentiation.Tissue barriers · 2022Article
- Recent Advances in the Role of Nuclear Factor Erythroid-2-Related Factor 2 in Spinal Cord Injury: Regulatory Mechanisms and Therapeutic Options.Frontiers in aging neuroscience · 2022Review
- Recent progress (2015-2020) in the investigation of the pharmacological effects and mechanisms of ginsenoside RbJournal of ginseng research · 2022Review
- Role of ginseng in the neurovascular unit of neuroinflammatory diseases focused on the blood-brain barrier.Journal of ginseng research · 2021Article
- Taurine and Ginsenoside Rf Induce BDNF Expression in SH-SY5Y Cells: A Potential Role of BDNF in Corticosterone-Triggered Cellular Damage.Molecules (Basel, Switzerland) · 2020Article
- Role of Connexins 30, 36, and 43 in Brain Tumors, Neurodegenerative Diseases, and Neuroprotection.Cells · 2020Review
- Effects of ginsenoside Rb1 on oxidative stress injury in rat spinal cords by regulating the eNOS/Nrf2/HO-1 signaling pathway.Experimental and therapeutic medicine · 2018Article
- Inhibition of Autophagy is Involved in the Protective Effects of Ginsenoside Rb1 on Spinal Cord Injury.Cellular and molecular neurobiology · 2018Article
- Correlation between connexin and traumatic brain injury in patients.Brain and behavior · 2017Article
- Natural Compounds as a Therapeutic Intervention following Traumatic Brain Injury: The Role of Phytochemicals.Journal of neurotrauma · 2017Review
- Phosphorylation of astrocytic connexin43 by ERK1/2 impairs blood-brain barrier in acute cerebral ischemia.Cell & bioscience · 2017Article
- Connexins in the Central Nervous System: Physiological Traits and Neuroprotective Targets.Frontiers in physiology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ginsenosides are the major active components of ginseng, which have been proven to be effective in therapies for neurodegenerative diseases. Ginsenoside Rb1 (GS-Rb1) is the most abundant among all the identified ginsenosides and has been shown to exert neuroprotective effects, although the underlying molecular mechanisms remain unclear. Connexins are a family of transmembrane proteins that form gap junctions, which are important for diffusion of cytosolic factors such as ions and second messenger signaling molecules. Previous studies have shown that a subset of connexin proteins is involved in neuroprotection. We investigated the protective effects of GS-Rb1 against traumatic brain injury (TBI) and the potential mechanism using TBI mouse model. We discovered that TBI-induced brain injury and up-regulation of connexin40 (Cx40) protein expression as early as 6 h post-TBI, which was reversed by administration of GS-Rb1. In addition, we found that the protective effects of GS-Rb1 are dose and time dependent and are partially mediated through phosphorylation of ERK1/2 signaling pathway, as evidenced by the abolishment of GS-Rb1-mediated elevation of p-ERK1/2 expression and inhibition of Cx40 expressions when ERK inhibitor U0126 was used. Our study provides evidence that Cx40 is implicated in TBI-induced brain injuries, and GS-Rb1 exerts neuroprotective activity against TBI involving down-regulation of Cx40 expression.
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