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ORIGINAL ARTICLE
Year : 2018  |  Volume : 14  |  Issue : 58  |  Page : 489-494

Anti-neuro-inflammatory effects of the bioactive compound capsaicin through the NF-κB signaling pathway in LPS-stimulated BV2 microglial cells


1 Third Affiliated Hospital, Beijing University of Chinese Medicine, 51 Anwai Xiaoguan Street, ChaoYang District, Beijing, 100029, People's Republic of China
2 Neurology Department, Xuan Wu Hospital of Capital Medical University, 45 Changchun St. Beijing, 100053, People's Republic of China

Correspondence Address:
Miao Qu
Neurology Department, Xuan Wu Hospital of Capital Medical University, 45 Changchun St. Beijing, 100053
People's Republic of China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_73_18

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Background: Inflammation in the central nervous system, resulting from a loss of control involving a network of neuronal cells, is foremost contributors to the instigation and advancement of major neurodegenerative diseases. Therefore, therapeutic strategies should restore back to a well-controlled and finely-tuned balance of immune reactions, and protect neurons from inflammatory damage. Objective: The objective of this study is to evaluate the anti-neuroinflammatory potential of Capsaicin in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. Materials and Methods: In this present study, we selected Capsaicin and investigated through cell-based-assay systems through the various cellular techniques enzyme-linked immunosorbent, immunoblot and immunofluorescence assays to identify anti-inflammatory effects. Results: We found that capsaicin exhibited highly anti-inflammatory and neuroprotective effects in cell culture experiments, reduced nitric oxide, tumor necrosis factor-α, interleukin-1 β, and interleukin expression from activated BV-2 microglia cells dose-dependently. On the intracellular level, capsaicin inhibited IκB-phosphorylation and subsequently nuclear Factor-κB (NF-κB)-translocation in microglia cells. Further, capsaicin blocked the protein expressions of inducible nitric oxide synthase and cyclooxygenase-2. Further, capsaicin inhibits the increased production of pro-inflammatory responses in LPS-stimulated BV-2 cells by suppressing NF-κB activation. Conclusion: The significant inhibition of neuroinflammatory responses in stimulated microglial cells together indicate that capsaicin is a potential therapeutic agent and could possibly be used in the development of novel drug for the prevention and treatment of neuroinflammatory diseases. Abbreviations used: CNS: Central Nervous System; iNOS: Inducible nitric oxide synthase; COX-2: Cyclooxygenase; NF-κB: Nuclear factor kappa-light-chain-enhancer of activated B cells; LPS: Lipopolysaccharide; PGE2: Prostaglandin E2; NO: Nitric oxide; IL-6: Interleukin; IL-1 β-interleukin-1 β; TNF-α: Tumor necrosis factor-α


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