Artesunate Attenuates Lipopolysaccharide-Stimulated Proinflammatory Responses by Suppressing TLR4, MyD88 Expression, and NF-κB Activation in Microglial Cells

作者：Wang, Dunjing; Shi, Jun; Lv, Shuiqing; Xu, Weiwei; Li, Jizhen; Ge, Wei; Xiao, Chenghua; Geng, Deqin^*; Liu, Yonghai

来源：Inflammation, 2015, 38(5): 1925-1932.

DOI：10.1007/s10753-015-0172-7

• artesunate
• neuroinflammation
• microglia
• Toll-like receptor 4
• NF-kappa B

Microglia are considered as a major target in the prevention of neuroinflammation by modulating the production of pro-inflammatory mediators. Artesunate, a water-soluble artemisinin derivative, exerts an anti-inflammatory effect. In the present study, we showed artesunate dose-dependently suppressed the lipopolysaccharide (LPS)-induced production of nitric oxide (NO), inducible nitric oxide synthase (iNOS), and interleukin-1beta (IL-1 beta) in BV2 microglial cells. In addition, artesunate inhibited LPS-induced expression of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), and activation of nuclear factor kappa B (NF-kappa B) by blockade of inhibitor of NF-kappa B (I kappa B) degradation. This data indicate that artesunate attenuates the generation of proinflammatory mediators on LPS-stimulated BV-2 microglial cells. And this effect may be associated with the suppression of TLR4/MyD88/NF-kappa B signaling pathways. Therefore, artesunate may be a potential anti-neuroinflammatory agent.

• 出版日期2015-10
• 单位上海交通大学; 徐州医科大学