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Ginkgolide B Suppresses Methamphetamine-Induced Microglial Activation Through TLR4-NF-κB Signaling Pathway in BV2
Fen Wan1, Songsong Zang2, Guoqing Yu1
1Department of Neurology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, Jiangsu, China.
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.
Insights
Methamphetamine (Meth) exposure activates microglial cells by increasing Toll-like receptor 4 (TLR4) expression and neuroinflammation. Ginkgolide B (GB) can mitigate these effects, suggesting TLR4 as a therapeutic target for Meth-induced neuroinflammation.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglial cells show altered morphology and proliferation in methamphetamine (Meth) abuse.
- Mechanisms of Meth-induced microglial activation are not fully understood.
- Toll-like receptor 4 (TLR4) is implicated in inflammatory processes.
Purpose of the Study:
- To investigate if Meth treatment affects TLR4 expression in microglial cells.
- To evaluate the impact of ginkgolide B (GB) on Meth-mediated inflammation.
- To confirm the role of TLR4 in Meth-induced neuroinflammation.
Main Methods:
- BV2 microglial cells were treated with Meth.
- TLR4 expression and inflammatory cytokine (TNF-α, IL-6, IL-1β) release were measured.
- Cells were pre-treated with ginkgolide B (GB) or subjected to TLR4 knockdown via siRNA.
Main Results:
- Meth treatment significantly upregulated TLR4 expression and activated the NF-κB pathway.
- Meth increased the release of TNF-α, IL-6, and IL-1β.
- GB pre-treatment partially attenuated these Meth-induced inflammatory effects.
- TLR4 knockdown via siRNA significantly reduced Meth-mediated inflammatory responses.
Conclusions:
- Methamphetamine exposure activates microglial cells, associated with TLR4 upregulation and NF-κB pathway activation.
- Ginkgolide B attenuates Meth-induced neuroinflammation, partly via the TLR4-NF-κB pathway.
- Targeting TLR4 presents a potential therapeutic strategy for Meth-induced neuroinflammation.
