ArticleMolecular neurobiology2014
Ginsenoside Re rescues methamphetamine-induced oxidative damage, mitochondrial dysfunction, microglial activation, and dopaminergic degeneration by inhibiting the protein kinase Cδ gene.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 111 citations in OpenAlex.
- Targeting glial cells: Unveiling the neuroprotective mechanisms of Ginseng in the brain microenvironment.Acta pharmaceutica Sinica. B · 2026Review
- Up-regulation of Oxidative Burden, NFκB, and D1 Receptor Is Involved in the Neuropsychotoxic Behaviors Induced by Camfetamine, a New Psychoactive Substance; Involvements of the Neuromodulation by GPx-1 Gene.Neurochemical research · 2025Article
- Review
- Brain dysfunctions and neurotoxicity induced by psychostimulants in experimental models and humans: an overview of recent findings.Neural regeneration research · 2024Article
- Inhibition of PKC-δ retards kidney fibrosis via inhibiting cGAS-STING signaling pathway in mice.Cell death discovery · 2024Article
- Ginsenosides and Tumors: A Comprehensive and Visualized Analysis of Research Hotspots and Antitumor Mechanisms.Journal of Cancer · 2024Article
- A Review on the Disruption of Novel Object Recognition Induced by Methamphetamine.Addiction & health · 2023Review
- Mountain-cultivated ginseng protects against cognitive impairments in aged GPx-1 knockout mice via activation of Nrf2/ChAT/ERK signaling pathway.Journal of ginseng research · 2023Article
- α-Pinene Attenuates Methamphetamine-Induced Conditioned Place Preference in C57BL/6 Mice.Biomolecules & therapeutics · 2023Article
- Role of Microglia in Psychostimulant Addiction.Current neuropharmacology · 2023Review
- Ginsenoside Rg1 inhibits nucleus pulposus cell apoptosis, inflammation and extracellular matrix degradation via the YAP1/TAZ pathway in rats with intervertebral disc degeneration.Journal of orthopaedic surgery and research · 2022Article
- Effect of rottlerin on astrocyte phenotype polarization after trimethyltin insult in the dentate gyrus of mice.Journal of neuroinflammation · 2022Article
- Pharmacological Properties of Ginsenoside Re.Frontiers in pharmacology · 2022Review
- Neurotoxicity of methamphetamine: Main effects and mechanisms.Experimental neurology · 2021Review
- Ginsenoside Re Protects against Serotonergic Behaviors Evoked by 2,5-Dimethoxy-4-iodo-amphetamine in Mice via Inhibition of PKCδ-Mediated Mitochondrial Dysfunction.International journal of molecular sciences · 2021Article
- Methamphetamine-induced dopaminergic neurotoxicity as a model of Parkinson's disease.Archives of pharmacal research · 2021Review
- The Role of α-Synuclein in Methamphetamine-Induced Neurotoxicity.Neurotoxicity research · 2021Review
- Review of ginsenosides targeting mitochondrial function to treat multiple disorders: Current status and perspectives.Journal of ginseng research · 2021Review
- The Role of Chinese Herbal Therapy in Methamphetamine Abuse and its Induced Psychiatric Symptoms.Frontiers in pharmacology · 2021Review
- Natural Products in Modulating Methamphetamine-Induced Neuronal Apoptosis.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ginsenoside Re, one of the main constituents of Panax ginseng, possesses novel antioxidant and anti-inflammatory properties. However, the pharmacological mechanism of ginsenoside Re in dopaminergic degeneration remains elusive. We suggested that protein kinase C (PKC) δ mediates methamphetamine (MA)-induced dopaminergic toxicity. Treatment with ginsenoside Re significantly attenuated methamphetamine-induced dopaminergic degeneration in vivo by inhibiting impaired enzymatic antioxidant systems, mitochondrial oxidative stress, mitochondrial translocation of protein kinase Cδ, mitochondrial dysfunction, pro-inflammatory microglial activation, and apoptosis. These protective effects were comparable to those observed with genetic inhibition of PKCδ in PKCδ knockout (-/-) mice and with PKCδ antisense oligonucleotides, and ginsenoside Re did not provide any additional protective effects in the presence of PKCδ inhibition. Our results suggest that PKCδ is a critical target for ginsenoside Re-mediated protective activity in response to dopaminergic degeneration induced by MA.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.