2. Academic Validation
  3. Dexamethasone sodium phosphate attenuates lipopolysaccharide-induced neuroinflammation in microglia BV2 cells

Dexamethasone sodium phosphate attenuates lipopolysaccharide-induced neuroinflammation in microglia BV2 cells

  • Naunyn Schmiedebergs Arch Pharmacol. 2020 Sep;393(9):1761-1768. doi: 10.1007/s00210-019-01775-3.
Bin Hui 1 2,  Xin Yao 3,  Liping Zhang 4,  Qinhua Zhou 5
Affiliations

Affiliations

  • 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. [email protected].
  • 5 College of Medicine, Jiaxing University, Jiaxing, China. [email protected].
PMID: 31915845 DOI: 10.1007/s00210-019-01775-3
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 LPS-activated 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

Chemokine; Cytokine; Dexamethasone sodium phosphate; LPS; Microglia.

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