Artemisinin inhibits lipopolysaccharide-induced interferon-beta production in RAW 264.7 cells: implications on signal transducer and activator of transcription-1 signaling and nitric oxide production
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- Artemisinin inhibits lipopolysaccharide-induced interferon-beta production in RAW 264.7 cells: implications on signal transducer and activator of transcription-1 signaling and nitric oxide production
- Ki Hwan Park; Yeo Dae Yoon; S B Han; Soo Jin Oh; Jieun Yun; Chang Woo Lee; K Lee; S K Park; H M Kim; Jong Soon Kang
- Bibliographic Citation
- International Immunopharmacology, vol. 14, no. 3, pp. 580-584
- Publication Year
- Artemisinin is a well-known anti-malarial drug and has been shown to inhibit nitric oxide (NO) production. In this study, we investigated the effect of artemisinin on lipopolysaccharide (LPS)-induced production of IFN-β and characterized the potential relationship between artemisinin-mediated inhibition of IFN-β and NO production. Artemisinin suppressed IFN-β production and mRNA expression in a dose-dependent manner in LPS-stimulated RAW 264.7 cells. LPS-induced phosphorylation of signal transducer and activator of transcription-1 (STAT-1) was also inhibited by artemisinin treatment in RAW 264.7 cells. In addition, artemisinin suppressed LPS-induced production of NO in RAW 264.7 cells. Further study demonstrated that artemisinin-mediated inhibition of NO production and STAT-1 phosphorylation was reversed by addition of exogenous IFN-β. Moreover, artemisinin does not affect IFN-β-induced STAT-1 phosphorylation in RAW 264.7 cells. Collectively, these results suggest that the inhibition of IFN-β production by artemisinin and concomitant attenuation of STAT-1 activation might be involved in artemisinin-mediated inhibition of NO production in macrophages.
- Artemisinin; IFN-β; Nitric oxide; STAT-1
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- Ochang Branch Institute > Division of Bioinfrastructure > Laboratory Animal Resource Center > 1. Journal Articles
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