期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 15, 期 2, 页码 296-302出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2012.12.005
关键词
Britanin; Inducible NO synthase (iNOS); Cyclooxygenase (COX)-2; Pro-inflammatory cytokines; Nuclear factor (NF)-kappa B; Mitogen-activated protein (MAP) kinases
资金
- Ministry of Health & Welfare, Republic of Korea [B0800023, A111092]
- Korea Health Promotion Institute [A111092] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Little is known about the biological properties of britanin, which is isolated from the flowers of Inula japonica (Inulae Flos). Based on our previous studies that Inulae Flos had anti-inflammation and anti-asthmatic activities, we tried to find the bioactive compounds from it. In this study, the anti-inflammatory effects of britanin on the inflammatory mediators as well as on nuclear factor (NF)-kappa B and mitogen-activated protein (MAP) kinase activation were evaluated in RAW 264.7 cells. Britanin inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE(2)) along with the expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. In addition, britanin reduced the release of pro-inflammatory cytokines, such as TNF-alpha, IL-1 beta, and IL-6. Furthermore, the phosphorylations of MAP kinases (p38 and JNK) in LPS-stimulated RAW 264.7 cells were suppressed by britanin. Moreover, britanin inhibited the NF-kappa B activation induced by LPS, which was associated with the abrogation of Met degradation and subsequent decreases in nuclear p65 levels. This study suggests that the anti-inflammatory activities of britanin might be attributed to the inhibition of iNOS and COX-2 and cytokine expression at least in part, through the attenuation of the phosphorylations of MAP kinases and NF-kappa B activation via I kappa B alpha degradation in macrophages. We conclude that britanin may have potential for the treatment of inflammatory diseases through the down-regulation of MAP kinases and NF-kappa B mediated activation of macrophages. (C) 2012 Elsevier B.V. All rights reserved.
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