Journal
LIFE SCIENCES
Volume 88, Issue 25-26, Pages 1121-1126Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.lfs.2011.04.011
Keywords
Eupatilin; Nuclear factor-kappa B; Inflammation; Pro-inflammatory mediator; Macrophages
Funding
- Ministry for Health, Welfare & Family Affairs, Republic of Korea [A090015]
- Korea government (MEST) [R01-2008-000-20037-0]
- Korean Ministry of Education, Science and Technology
- Korea Health Promotion Institute [A090015] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [R01-2008-000-20037-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Aims: Eupatilin (5,7-dihydroxy-3,4,6-trimethoxyflavone) is a pharmacologically active ingredients in Stillen (TM), a drug for the gastric mucosal ulcers. Eupatilin has been known to possess anti-peptic, anti-cancer, and anti-allergy activity. In this report, we defined the effect of eupatilin on the endotoxin-induced inflammation in lipopolysaccharide (LPS)-stimulated macrophages. Main methods: Mouse J774A.1 cell line and mouse peritoneal macrophages were used. Gene expression and production of inflammatory mediators were determined by real-time PCR and Western blot Key findings: Eupatilin dose-dependently suppressed LPS-induced expression of inducible nitric oxide synthase (iNOS) and production of nitric oxide (NO). Eupatilin decreased LPS-induced expression of inflammatory mediators and pro-inflammatory cytokines such as cyclooxygenase-2, monocyte chemoattractant protein-1, tumor necrosis factor-alpha, interleukin (IL)-1 beta and IL-6. In addition, this suppression of inflammatory mediators was nuclear factor (NF)-kappa B dependent. Significance: Our findings imply that eupatilin suppresses inflammatory responses by the inhibition of NF-kappa B signaling pathway, and downstream inflammatory mediators in endotoxin-stimulated macrophages. (C) 2011 Elsevier Inc. All rights reserved.
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