Anti-neuro-inflammatory Effects of the Bioactive Compound Capsaicin through the NF-κB Signaling Pathway in LPS- Stimulated BV2 Microglial Cells

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.