Pectolinarin inhibited LPS-stimulated inflammation in microglial BV2 cells via NF-KB signaling pathway

Background: Neuro-inflammation is regarded as one of the critical pathogenesis in neurodegenerative diseases, which is characterized by the activated microglial cells. Pectolinarin (Pec), a natural flavonoid that exists in many Chinese herbal medicines, has been reported to have various biological activities. However, the effects and mechanisms on neuro-inflammation are not clear. Methods: In this study, the inhibitory effects and mechanisms of Pec on neuro-inflammation were investigated in the LPS-stimulated microglial BV 2 cells. BV 2 microglial cells were treated with Pec or vehicle, followed by LPS. Enzyme -linked immunosorbent assay, real-time quantitative PCR, nitric oxide and reactive oxygen species assay, and western blot were performed to examine the effects of Pec on neuro-inflammatory responses. Results: We showed that Pec significantly inhibited the expression of tumor necrosis factor alpha and interleukin 6 in mRNA and protein levels induced by LPS. Moreover, the production of nitric oxide, iNOS, reactive oxygen species, and COX -2 were suppressed by Pec in LPS-stimulated microglial BV 2 cells. In addition, Pec inhibited LPS-induced inflammation via nuclear factor kappa B signaling pathway, as evidenced by the reduction of the phosphorylation of inhibitor of nuclear factor kappa -B kinase, the degradation of I kappa B alpha, and the nuclear translocation of p65. Conclusion: Taken together, Pec exhibited anti-inflammatory effects in LPS-stimulated microglial BV 2 cells via nuclear factor kappa B signaling pathway, which might provide therapeutic potential for neuro-inflammation and neurodegenerative diseases.