Thromboxane A2 receptor antagonist SQ29548 suppresses the LPS‑induced release of inflammatory cytokines in BV2 microglia cells via suppressing MAPK and NF‑κB signaling pathways

Yan,Aijuan; Cai,Gaoyu; Xia,Weiliang; Fu,Yi

doi:10.3892/mmr.2017.6884

Thromboxane A2 receptor antagonist SQ29548 suppresses the LPS‑induced release of inflammatory cytokines in BV2 microglia cells via suppressing MAPK and NF‑κB signaling pathways

Authors:
- Aijuan Yan
- Gaoyu Cai
- Weiliang Xia
- Yi Fu
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Affiliations: Department of Neurology and Institute of Neurology, Rui Jin Hospital, Shanghai Jiao Tong University, Shanghai 200025, P.R. China, School of Biomedical Engineering and Med‑X Research Institute, Shanghai Jiao Tong University, Shanghai 200030, P.R. China
Published online on: June 29, 2017 https://doi.org/10.3892/mmr.2017.6884
Pages: 2491-2496
Copyright: © Yan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Inflammation in the brain, characterized by the activation of microglia, is hypothesized to participate in the pathogenesis of neuronal disorders. It is proposed that thromboxane A2 receptor (TXA2R) activation is involved in thrombosis/hemostasis and inflammation responses. In the present study, the anti‑inflammatory effects of SQ29548 on lipopolysaccharide (LPS)‑stimulated BV2 microglial cells and its molecular mechanisms were investigated. In the BV2 cell line, LPS‑stimulated nitric oxide (NO) and inflammatory cytokine release, and the phosphorylation of mitogen‑activated protein kinases (MAPKs) and the nuclear factor (NF)‑κB were assessed using an NO assay kit, reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. In vitro studies demonstrated that SQ29548 inhibited LPS‑stimulated BV2 activation and reduced the mRNA expression levels of interleukin (IL)‑1β, IL‑6, tumor necrosis factor‑α and inducible NO synthase via inhibition of MAPKs and the NF‑κB signaling pathway. SQ29548 inhibited the LPS‑induced inflammatory response by blocking MAPKs and NF‑κB activation in BV2 microglial cells.

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