Monascin ameliorate inflammation in the lipopolysaccharideinduced BV-2 microglial cells via suppressing the NF-κB/p65 pathway

Objective(s): The pathophysiology of neurodegenerative diseases is complicated, in which inflammatory reactions play a vital role. Microglia cells activation, an essential process of neuroinflammation, can produce neurotoxic molecules and neurotrophic factors, which aggravate inflammation and neuronal injury. Monascin, a major component of red yeast rice, is an azaphilonoid pigment with potential antiinflammatory effects; however, the effects in central nervous system have not been evaluated. Our goal in this project was to explore the therapeutic effect and the underlying mechanism of Monascin, which may be via anti-inflammatory action. Materials and Methods: We used lipopolysaccharide to induce BV-2 microglial cells in order to form an inflammation model in vitro. The anti-inflammatory effects of Monascin were measured by enzymelinked immunosorbent assay (ELISA), real time-polymerase chain reaction (RT-PCR), Western Blot and Immunofluorescent staining. Results: Our data indicated that inflammatory cytokines including interleukin-1β (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α) and nitric oxide were suppressed by Monascin treatment. Furthermore, the related pro-inflammatory genes were inhibited consistent with the results of ELISA assay. Western blotting results showed that the phosphorylation of nuclear factor kappa B (NF-κB/p65) was reduced by Monascin treatment may be through suppressing the activation of IκB. Furthermore, immunofluorescence staining showed that the translocation of NF-κB/p65 to the cellular nuclear was blockaded after Monascin treatment. Conclusion: Taken together, Monascin exerts anti-inflammatory effect and suppressed microglia activation, which suggested its potential therapeutic effect for inflammation-related diseases.