Brilliant blue G attenuates neuro‑inflammation via regulating MAPKs and NF‑κB signaling pathways in lipopolysaccharide‑induced BV2 microglia cells
- Wei Wang
- Feiran Huang
- Weifeng Jiang
- Weiwei Wang
- Jie Xiang
Affiliations: Department of Rehabilitation, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China, Department of Neurology, The Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, P.R. China, Department of Neurology, The Second People's Hospital of Quzhou, Quzhou, Zhejiang, 324000, P.R. China
- Published online on: September 18, 2020 https://doi.org/10.3892/etm.2020.9244
Copyright: © Wang
et al. This is an open access article distributed under the
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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.