Brilliant blue G attenuates neuro-inflammation via regulating MAPKs and NF-κB signaling pathways in lipopolysaccharide-induced BV2 microglia cells.

Abstract

Previous studies have demonstrated that the P2X purinoceptor 7 (P2X7) receptor (P2X7R) serves a critical role in regulating the inflammatory response of various diseases in the central nervous system. The anti-inflammatory effect of brilliant blue G (BBG), a specific antagonist of the P2X7R, remains unclear in lipopolysaccharide (LPS)-induced BV-2 cells. The present study suggested that BBG attenuated the neuroinflammatory response; the protein levels of inducible oxide synthase and cyclooxygenase-2, and the mRNA and secretion levels of pro-inflammatory cytokines including interleukin (IL)-16, IL-1β and tumor necrosis factor-α (TNF-α), were all decreased in LPS-induced BV2 cells. BBG inhibited the activation of MAPKs by inhibiting the phosphorylation of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase and extracellular signal-regulated kinase. Notably, transcription factor p65 nuclear translocation was also inhibited, thereby leading to the inactivation of NF-κB. The inhibitory effects of BBG on MAPKs and NF-κB were additionally enhanced through the application of MAPK and NF-κB inhibitors. Taken together, the results demonstrated that BBG contributed to the suppression of the inflammatory effects in LPS-induced BV2 cells via the inhibition of NF-κB and MAPKs signaling pathways.