Title of article
Baicalein inhibits lipid accumulation by regulating early adipogenesis and m-TOR signaling
Author/Authors
Seo، نويسنده , , Min Jung and Choi، نويسنده , , Hyeon-Son and Jeon، نويسنده , , Hui-Jeon and Woo، نويسنده , , Mi-Seon and Lee، نويسنده , , Boo-Yong، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2014
Pages
8
From page
57
To page
64
Abstract
Baicalein is a type of flavonoid that originates from Scutellaria baicalensis. In this study, we examined how baicalein inhibits lipid accumulation during adipogenesis in 3T3-L1 cells. Our data show that baicalein inhibited lipid accumulation during adipogenesis in a dose-dependent manner. Baicalein inhibition was limited to the early adipogenic stage. Cell cycle analysis showed that baicalein induced cell cycle arrest in the G0/G1 phase through cyclin downregulation. In addition, baicalein suppressed the mRNA expression of early adipogenic factors leading to downregulation of late adipogenic factors at mRNA and protein levels. Inhibition of adipogenic factors by baicalein was correlated with downregulation of lipid synthetic enzymes. Additionally, baicalein negatively regulated the m-TOR signaling pathway involved in lipid accumulation during adipogenesis, thus inhibiting phosphorylation of m-TOR and p70S6 K. In a zebrafish study, baicalein significantly reduced lipid accumulation in Nile Red staining. Consistent with a report using cell lines, mRNA expression of adipogenic factors was decreased in a dose-dependent manner by baicalein. This result reflects a reduction in total triglyceride levels based on a triglyceride assay. Our data suggest that baicalein inhibits lipid accumulation by controlling the cell cycle and m-TOR signaling in 3T3-L1 cells, and its anti-adipogenic effect was found in a zebrafish model.
Keywords
Triglyceride signaling pathway , Adipogenesis , m-TOR signaling pathway , Mitotic clonal expansion , 3T3-L1 , zebrafish
Journal title
Food and Chemical Toxicology
Serial Year
2014
Journal title
Food and Chemical Toxicology
Record number
2126898
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