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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Artemisia, Blotting, Western, Cell Culture Techniques, Cell Line, Cell Survival, Cytokines, Dose-Response Relationship, Drug, Flavonoids, Gene Expression, Inflammation Mediators, Lipopolysaccharides, Macrophages, Peritoneal, Mice, Mice, Inbred BALB C, Molecular Structure, NF-kappa B, Nitric Oxide, Nitric Oxide Synthase Type II, Reverse Transcriptase Polymerase Chain Reaction.
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Does eupatilin inhibit lipopolysaccharide-induced expression of inflammatory mediators in macrophages? Context: 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. 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. 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-α, interleukin (IL)-1β and IL-6. In addition, this suppression of inflammatory mediators was nuclear factor (NF)-κB dependent.
assistant
Our findings imply that eupatilin suppresses inflammatory responses by the inhibition of NF-κB signaling pathway, and downstream inflammatory mediators in endotoxin-stimulated macrophages. Final Decision: yes