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Food Funct. 2016 Jul 13;7(7):3263-72. doi: 10.1039/c6fo00540c.

Protective effect of Tremella fuciformis Berk extract on LPS-induced acute inflammation via inhibition of the NF-κB and MAPK pathways.

Author information

1
Food Biotechnology Program, Korea University of Science and Technology, Daejeon 305-350, Republic of Korea.
2
Division of Functional Food Research, Korea Food Research Institute, Gyeonggi-do, 463-746, Republic of Korea. hyunku@kfri.re.kr skjung@kfri.re.kr.
3
Division of Nutrition and Metabolism Research, Korea Food Research Institute, Gyeonggi-do, 463-746, Republic of Korea.
4
Food Biotechnology Program, Korea University of Science and Technology, Daejeon 305-350, Republic of Korea and Division of Functional Food Research, Korea Food Research Institute, Gyeonggi-do, 463-746, Republic of Korea. hyunku@kfri.re.kr skjung@kfri.re.kr.
5
Food Safety Center, Ottogi Corp, Gyeonggi-do, 431-070, Republic of Korea.

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.

PMID:
27334265
DOI:
10.1039/c6fo00540c
[Indexed for MEDLINE]

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