ArticleNeurochemical research2017
Ginkgolide B Suppresses Methamphetamine-Induced Microglial Activation Through TLR4-NF-κB Signaling Pathway in BV2 Cells.
Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 40 citations in OpenAlex.
- Transcription factors implicated in substance use disorder, from immediate early genes to altered gene expression.Brain research · 2026Review
- Ibudilast-Mediated Suppression of Neuronal TLR4 in the Prefrontal Cortex Mitigates Methamphetamine-Induced Neuroinflammation and Addictive Behaviours.Addiction biology · 2025Article
- Therapeutic targeting of neuroinflammation in methamphetamine use disorder.Future medicinal chemistry · 2025Review
- Microglia in neuroimmunopharmacology and drug addiction.Molecular psychiatry · 2024Review
- The Effectiveness of Mindfulness in the Treatment of Methamphetamine Addiction Symptoms: Does Neuroplasticity Play a Role?Brain sciences · 2024Review
- Oxidative Stress and Inflammatory Biomarkers in People with Methamphetamine Use Disorder.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2023Article
- Role of Microglia in Psychostimulant Addiction.Current neuropharmacology · 2023Review
- The Crosstalk Between Neurons and Glia in Methamphetamine-Induced Neuroinflammation.Neurochemical research · 2022Review
- The Role of Chinese Herbal Therapy in Methamphetamine Abuse and its Induced Psychiatric Symptoms.Frontiers in pharmacology · 2021Review
- Methamphetamine-Induced Neuronal Damage: Neurotoxicity and Neuroinflammation.Biomolecules & therapeutics · 2020Review
- Role of Ginkgolides in the Inflammatory Immune Response of Neurological Diseases: A Review of Current Literatures.Frontiers in systems neuroscience · 2020Article
- Methamphetamine Activates Toll-Like Receptor 4 to Induce Central Immune Signaling within the Ventral Tegmental Area and Contributes to Extracellular Dopamine Increase in the Nucleus Accumbens Shell.ACS chemical neuroscience · 2019Article
- Effect of methamphetamine on the fasting blood glucose in methamphetamine abusers.Metabolic brain disease · 2018Article
- Cardioprotection of Ginkgolide B on Myocardial Ischemia/Reperfusion-Induced Inflammatory Injury via Regulation of A20-NF-κB Pathway.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Accumulating evidence suggests that microglial cells have altered morphology and proliferation in different brain regions of methamphetamine (Meth) abusers and Meth-abusing animal models. However, the possible mechanisms underlying Meth-induced microglial activation remain poorly understood. Meanwhile, Toll-like receptor4 (TLR4) is closely associated with inflammation. Therefore the aim of the present study was to assess whether Meth treatment affects TLR4 expression; in addition, we evaluated the effects of ginkgolide B (GB), a diterpene lactone extracted from Ginkgo biloba, on Meth-mediated inflammation. BV2 cells were treated with Meth. Interestingly, Meth treatment significantly increased TLR4 expression, activated the NF-κB signaling pathway, and promoted TNF-α, IL-6 and IL-1β excretion. These effects, however, were partially attenuated by GB pre-treatment. To further confirm the role of TLR4 in Meth-mediated inflammation, the siRNA technology was applied to knock down TLR4, which resulted in hampered Meth-mediated inflammatory responses, confirming the important role of TLR4 in this process. Taken together, our findings suggested that Meth exposure results in BV2 cell activation, in association with TLR4 upregulation. GB could attenuate Meth-induced inflammation, at least partially through TLR4-NF-κB signaling pathway, therefore, targeting TLR4 may constitute a potential intervention strategy for Meth mediated neuroinflammation.
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