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Inhibitory Effects of Butein on Adipocyte Differentiation through Upregulation of Nrf‐2/HO‐1 Pathway in 3T3‐L1 Adipocyte
Author(s) -
Lee Junsoo,
Yang Jinwoo
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.917.1
Subject(s) - adipocyte , adipogenesis , chemistry , downregulation and upregulation , 3t3 l1 , peroxisome proliferator activated receptor , transcription factor , peroxisome , pharmacology , microbiology and biotechnology , biochemistry , receptor , adipose tissue , biology , gene
Butein is the biologically active component of Toxicodendron vernicifluum and has been shown to have pleiotropic effects such as induction of apoptosis, anti‐cancer, anti‐fibrogenic, and anti‐inflammatory activities. In this study, the effects of butein on adipocyte differentiation and the mechanisms involved were investigated in 3T3‐L1 adipocyte. The treatment of butein inhibited the protein expression of key transcription factors such as CCAAT‐enhancer‐binding proteins α (C/EBPα) and peroxisome proliferator‐activated receptor γ (PPARγ). Butein also increased Nrf‐2 and HO‐1 protein expressions in a dose‐dependent manner. Treatment with zinc protoporphyrin (ZnPP), a specific inhibitor of HO‐1, abolished the inhibitory effects of butein on the C/EBPα and PPARγ protein expressions. Furthermore, transfection of Nrf2 siRNA significantly reversed the butein‐mediated increase of HO‐1 protein expression and decrease of C/EBPα and PPARγ protein expressions. In conclusion, butein inhibited the adipogenesis in 3T3‐L1 adipocyte through, at least in part, upregulation of Nrf‐2/HO‐1 signaling pathway. These results suggest that butein has preferable properties for obesity or metabolic syndrome.