Effect of artemisinin on the release of inflammatory mediators of LPS-activated microglia

Objective To investigate the effect of artemisinin (ART) on the release of inflammatory mediators induced by lipopolysaccharide (LPS) in microglia, and to investigate the inhibitory effect of artemisinin on the inflammatory response of neurons in Parkinson' s disease and its mechanism. Methods The concentration of ART on BV2 microglia was detected by CCK8 method. LPS-induced microglia was treated with a given ART drug concentration. The effects of ART on the proinflammatory factors interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were detected by quantitative PCR and ELISA. Western blot was used to detect the expression of NF-κB protein (P65) and IKBα, and the effect of ART on the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) genes. Results A dosage range of 0.1 to 10 μmol/L ART did not show a significant toxicity to BV2 cells, so 1 μmol/L ART was selected for further experiments. Quantitative PCR results showed that the expression of pro-inflammatory factors IL-1β and TNF-α mRNA was significantly decreased in the ART pretreatment group. The results of Western blotting showed that the expression levels of NF-κB and IKBα in the ART pretreatment group were significantly increased, and the expression levels of inflammation-inducing enzymes iNOS and COX-2 were significantly decreased. Conclusion ART can regulate the expression of inflammatory factors and inflammation-inducing enzymes in LPS-activated BV2 microglia and exert anti-inflammatory effects, which may be achieved by regulating NF-κB signaling pathway.