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Benfotiamine attenuates inflammatory response in LPS stimulated BV-2 microglia
Iva Bozic1, Danijela Savic1, Danijela Laketa2
1Department of Neurobiology, Institute for Biological Research "Sinisa Stankovic", University of Belgrade, Belgrade, Serbia.
Abstract:
Microglial cells are resident immune cells of the central nervous system (CNS), recognized as key elements in the regulation of neural homeostasis and the response to injury and repair. As excessive activation of microglia may lead to neurodegeneration, therapeutic strategies targeting its inhibition were shown to improve treatment of most neurodegenerative diseases. Benfotiamine is a synthetic vitamin B1 (thiamine) derivate exerting potentially anti-inflammatory effects. Despite the encouraging results regarding benfotiamine potential to alleviate diabetic microangiopathy, neuropathy and other oxidative stress-induced pathological conditions, its activities and cellular mechanisms during microglial activation have yet to be elucidated. In the present study, the anti-inflammatory effects of benfotiamine were investigated in lipopolysaccharide (LPS)-stimulated murine BV-2 microglia. We determined that benfotiamine remodels activated microglia to acquire the shape that is characteristic of non-stimulated BV-2 cells. In addition, benfotiamine significantly decreased production of pro-inflammatory mediators such as inducible form of nitric oxide synthase (iNOS) and NO; cyclooxygenase-2 (COX-2), heat-shock protein 70 (Hsp70), tumor necrosis factor alpha α (TNF-α), interleukin-6 (IL-6), whereas it increased anti-inflammatory interleukin-10 (IL-10) production in LPS stimulated BV-2 microglia. Moreover, benfotiamine suppressed the phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK) and protein kinase B Akt/PKB. Treatment with specific inhibitors revealed that benfotiamine-mediated suppression of NO production was via JNK1/2 and Akt pathway, while the cytokine suppression includes ERK1/2, JNK1/2 and Akt pathways. Finally, the potentially protective effect is mediated by the suppression of translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in the nucleus. Therefore, benfotiamine may have therapeutic potential for neurodegenerative diseases by inhibiting inflammatory mediators and enhancing anti-inflammatory factor production in activated microglia.
Insights
Benfotiamine, a vitamin B1 derivative, reduces inflammation in activated microglia by inhibiting pro-inflammatory mediators and signaling pathways. This suggests benfotiamine
Area of Science:
- Neuroscience and Immunology
- Cellular Biology
- Pharmacology
Background:
- Microglial cells are crucial for central nervous system (CNS) homeostasis and repair.
- Excessive microglial activation contributes to neurodegeneration, making inhibition a therapeutic target.
- Benfotiamine (vitamin B1 derivative) shows anti-inflammatory potential but its role in microglial activation is unclear.
Purpose of the Study:
- To investigate the anti-inflammatory effects of benfotiamine on lipopolysaccharide (LPS)-stimulated murine BV-2 microglia.
- To elucidate the cellular mechanisms underlying benfotiamine's action in activated microglia.
Main Methods:
- Murine BV-2 microglia were stimulated with LPS to induce activation.
- Benfotiamine treatment was applied, and its effects on microglial morphology were assessed.
- Production of pro-inflammatory and anti-inflammatory mediators (e.g., iNOS, NO, TNF-α, IL-6, IL-10) was measured.
- Key signaling pathways (ERK1/2, JNK, Akt, NF-κB) and their phosphorylation states were analyzed.
Main Results:
- Benfotiamine reverted activated microglia to a non-stimulated morphology.
- It significantly reduced pro-inflammatory mediators (iNOS, NO, COX-2, Hsp70, TNF-α, IL-6) and increased anti-inflammatory IL-10.
- Benfotiamine suppressed ERK1/2, JNK, and Akt phosphorylation, and inhibited NF-κB translocation.
- Suppression of NO involved JNK1/2 and Akt pathways; cytokine suppression involved ERK1/2, JNK1/2, and Akt.
Conclusions:
- Benfotiamine exhibits significant anti-inflammatory effects on activated microglia.
- Its mechanisms involve modulating inflammatory mediator production and inhibiting key signaling pathways (JNK, Akt, ERK, NF-κB).
- Benfotiamine holds therapeutic potential for neurodegenerative diseases by mitigating microglial-driven inflammation.
