The Effect Of Artemisinin On Release Of Inflammatory Mediators Of LPS-activated Microglia

Objective Bv2 microglia induced by lipopolysaccharide(LPS)were used to establish the cellular model of inflammatory response in chronic neurodegenerative diseases.In order to study the inhibitory effect of artemisinin on neuroinflammatory response in chronic neurodegenerative diseases and its mechanism,the effect of Artemisinin(ART)on the release of inflammatory mediators in this model was investigated by cell biology,molecular biology and immunohistochemistry.Methods BV2 cells,which were in good logarithmic growth state,were used for further experiment by routine culture of mouse BV2 microglia.BV2 microglia induced by lipopolysaccharide(LPS)were treated with different concentrations of artemisinin(ART).CCK8 assay was used to detect the concentration of ART on BV2 microglia.The effects of ART on the secretion of IL-1? and TNF-? were detected by ELISA.Western blot was used to detect the expression of NF-?B(p65),IKB? and the effect of ART on the gene expression of inducible nitric oxide synthase(i NOS)and cyclooxygenase 2(COX-2).Results CCK8 assay showed that ART had no obvious toxicity to BV2 microglia when the dose range was 0.1 to 10 ?mol/L.For the convenience of further experimental operation,1 ?mol/L was selected as the effective concentration of ART.ELISA results showed that the secretion levels of pro-inflammatory factors IL-1? and TNF-? in BV2 microglia pretreated with ART were significantly decreased.Western blot results showed that in ART pretreatment group,the expression levels of NF-?B(p65)and IKB? protein were significantly increased,while the expression level of inflammation-induced enzyme i NOS and COX-2 was significantly decreased.Conclusion ART can regulate the secretion of inflammatory factors and the expression of inflammatory inducers in BV2 microglia activated by LPS,and play an anti-inflammatory role,which may be achieved by regulating the signal pathway of NF-?B.