Dexamethasone sodium phosphate attenuates lipopolysaccharide-induced neuroinflammation in microglia BV2 cells
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ORIGINAL ARTICLE
Dexamethasone sodium phosphate attenuates lipopolysaccharide-induced neuroinflammation in microglia BV2 cells Bin Hui 1,2 & Xin Yao 3 & Liping Zhang 4 & Qinhua Zhou 5 Received: 27 July 2018 / Accepted: 9 October 2019 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Abnormal neuroinflammation ignited by overproduction of chemokines and cytokines via microglial cells can induce the occurrence and development of neurodegenerative disorders. The aim of this study is to investigate the effects of dexamethasone sodium phosphate (Dex-SP) on chemokine and cytokine secretion in lipopolysaccharide (LPS)-activated microglial cells. LPS markedly enhanced the secretion of pro-inflammatory factors such as regulated on activation, normal T cell expressed and secreted (RANTES), transforming growth factor beta-β1 (TGF-β1) and nitric oxide (NO), but decreased the production of macrophage inflammatory protein-1α (MIP-1α) and interleukin 10 (IL-10) in BV-2 microglial cells. Furthermore, LPS increased BV-2 microglial cell migration. However, Dex-SP treatment had the opposite effect, dampening the secretion of RANTES, TGF-β1, and NO, while increasing the production of MIP-1α and IL-10 and blocking migration of LPS-stimulated BV-2 microglial cells. Furthermore, Dex-SP markedly suppressed the LPS-induced degradation of IRAK-1 and IRAK-4, and blocked the activation in TRAF6, p-TAK1, and p-JNK in BV-2 microglial cells. These results showed that Dex-SP inhibited the neuroinflammatory response and migration in LPSactivated BV-2 microglia by inhibiting the secretion of RANTES, TGF-β1, and NO and increasing the production of MIP-1α and IL-10. The molecular mechanism of Dex-SP may be associated with inhibition of TRAF6/TAK-1/JNK signaling pathways mediated by IRAK-1 and IRAK-4. Keywords Dexamethasone sodium phosphate . Microglia . LPS . Chemokine . Cytokine
Introduction Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00210-019-01775-3) contains supplementary material, which is available to authorized users. * Liping Zhang [email protected] * Qinhua Zhou [email protected] 1
College of Pharmacy, Shanghai University of Medical & Health Sciences, Shanghai, China
2
Health School attached to Shanghai University of Medical & Health Sciences, Shanghai, China
3
Jiyuan Shi People’s Hospital, Jiyuan, Henan, China
4
Department of Emergency Medicine, Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University, Shanghai, China
5
College of Medicine, Jiaxing University, Jiaxing, China
Neuroinflammation is a complex, specialized immune response to pathological processes or injury in the brain. Controlled neuroinflammation can be beneficial, while exaggerated neuroinflammation plays a fundamental role in the pathogenesis of neuronal dysfunction. The hallmark of neuroinflammation is the activation of microglia (Walker and Lue 2005; Kim and Joh 2006; Lopes 2016). Hyperactivation of microglia results in deleterious and progressive neuronal dysfunction by abn
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