کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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5833588 | 1122628 | 2012 | 5 صفحه PDF | دانلود رایگان |
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.
⺠Artemisinin inhibits LPS-induced IFN-β production. ⺠Artemisinin inhibits LPS-induced STAT1 phosphorylation. ⺠Artemisinin inhibits nitric oxide production. ⺠IFN-β/STAT1 signaling is involved in the inhibition of NO production by artemisinin.
Journal: International Immunopharmacology - Volume 14, Issue 4, December 2012, Pages 580-584