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
- Authors
- Park, Ki Hwan; Yoon, Yeo Dae; Han, Sang-Bae; Oh, Soo Jin; Yun, Jieun; Lee, Chang Woo; Lee, Kiho; Park, Song-Kyu; Kim, Hwan Mook; Kang, Jong Soon
- Issue Date
- Dec-2012
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- Artemisinin; IFN-beta; STAT-1; Nitric oxide
- Citation
- INTERNATIONAL IMMUNOPHARMACOLOGY, v.14, no.4, pp.580 - 584
- Journal Title
- INTERNATIONAL IMMUNOPHARMACOLOGY
- Volume
- 14
- Number
- 4
- Start Page
- 580
- End Page
- 584
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/15948
- DOI
- 10.1016/j.intimp.2012.09.012
- ISSN
- 1567-5769
- Abstract
- 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-beta and characterized the potential relationship between artemisinin-mediated inhibition of IFN-beta and NO production. Artemisinin suppressed IFN-beta 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-beta. Moreover, artemisinin does not affect IFN-beta-induced STAT-1 phosphorylation in RAW 264.7 cells. Collectively, these results suggest that the inhibition of IFN-beta production by artemisinin and concomitant attenuation of STAT-1 activation might be involved in artemisinin-mediated inhibition of NO production in macrophages. (c) 2012 Elsevier B.V. All rights reserved.
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