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5‐Hydroxyferulic acid methyl ester isolated from wasabi leaves inhibits 3T3‐L1 adipocyte differentiation
Author(s) -
Misawa Naoki,
Hosoya Takahiro,
Yoshida Shuhei,
Sugimoto Osamu,
YamadaKato Tomoe,
Kumazawa Shigenori
Publication year - 2018
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.6060
Subject(s) - adipocyte , adipogenesis , glut4 , biochemistry , phenylpropanoid , chemistry , downregulation and upregulation , gene expression , lipid droplet , cellular differentiation , intracellular , biology , gene , adipose tissue , biosynthesis , chromosomal translocation
To investigate the compounds present in wasabi leaves ( Wasabia japonica Matsumura) that inhibit the adipocyte differentiation, activity‐guided fractionation was performed on these leaves. 5‐Hydroxyferulic acid methyl ester ( 1 : 5‐HFA ester), one of the phenylpropanoids, was isolated from wasabi leaves as a compound that inhibits the adipocyte differentiation. Compound 1 suppressed the intracellular lipid accumulation of 3T3‐L1 cells without significant cytotoxicity. Gene expression analysis revealed that 1 suppressed the mRNA expression of 2 master regulators of adipocyte differentiation, PPARγ and C/EBPα. Furthermore, 1 downregulated the expression of adipogenesis‐related genes, GLUT4, LPL, SREBP‐1c, ACC, and FAS. Protein expression analysis revealed that 1 suppressed PPARγ protein expression. Moreover, to investigate the relationship between the structure and activity of inhibiting the adipocyte differentiation, we synthesized 12 kinds of phenylpropanoid analog. Comparison of the activity among 1 and its analogs suggested that the compound containing the substructure that possess a common functional group at the ortho position such as a catechol group exhibits the activity of inhibiting the adipocyte differentiation. Taken together, our findings suggest that 1 from wasabi leaves inhibits adipocyte differentiation via the downregulation of PPARγ.