1. Protective effect of Tremella fuciformis Berk extract on LPS-induced acute inflammation via inhibition of the NF-κB and MAPK pathways.
- Author
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Lee J, Ha SJ, Lee HJ, Kim MJ, Kim JH, Kim YT, Song KM, Kim YJ, Kim HK, and Jung SK
- Subjects
- Acute Disease, Animals, Biological Products pharmacology, Cyclooxygenase 2 genetics, Cyclooxygenase 2 metabolism, Cytokines metabolism, Gentisates pharmacology, Hydroxybenzoates pharmacology, Inflammation chemically induced, Lipopolysaccharides, Male, Mice, Mice, Inbred ICR, NF-kappa B antagonists & inhibitors, NF-kappa B genetics, Nitric Oxide Synthase Type II genetics, Nitric Oxide Synthase Type II metabolism, Parabens pharmacology, Phosphorylation, Polytetrafluoroethylene pharmacology, RAW 264.7 Cells, Anti-Inflammatory Agents pharmacology, Basidiomycota chemistry, Inflammation drug therapy, MAP Kinase Signaling System drug effects, NF-kappa B metabolism, Protective Agents pharmacology
- Abstract
Tremella fuciformis Berk (TFB) has long been used as a traditional medicine in Asia. Although TFB exhibits antioxidant and anti-inflammatory effects, the mechanisms of action responsible have remained unknown. We confirmed the anti-inflammatory effects of Tremella fuciformis Berk extract (TFE) in RAW 264.7 cells and observed significantly suppressed LPS-induced iNOS/NO and COX-2/PGE2 production. TFE also suppressed LPS-induced IKK, IkB, and p65 phosphorylation, as well as LPS-induced translocation of p65 from the cytosol. Additionally, TFE inhibited LPS-induced phosphorylation of MAPKs. In an acute inflammation study, oral administration of TFE significantly inhibited LPS-induced IL-1β, IL-6 and TNF-α production and iNOS and COX-2 expression. The major bioactive compounds from TFB extract were identified as gentisic acid, protocatechuic acid, 4-hydroxybenzoic acid, and coumaric acid. Among these compounds, protocatechuic acid showed the strongest inhibitory effects on LPS-induced NO production in RAW 264.7 cells. Overall, these results suggest that TFE is a promising anti-inflammatory agent that suppresses iNOS/NO and COX-2/PGE2 expression, as well as the NF-κB and MAPK signaling pathways.
- Published
- 2016
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