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KMID : 0613820110210091346
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Journal of Life Science
2011 Volume.21 No. 9 p.1346 ~ p.1353
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Inhibition of Adipocyte Differentiation through G1 Arrest by Extract of Sophora tonkinensis Gapnep in 3T3-L1 Preadipocytes
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Jeong Hyun-Young
Hyun Sook-Kyung
Choi Yung-Hyun
Kim Byung-Woo
Kwon Hyun-Ju
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Abstract
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Sophora tonkinensis Gapnep has been used as a traditional herbal medicine in oriental regions since ancient times. In this study, the effect and mechanism of the MeOH extract of Sophora tonkinensis Gapnep (STME) on adipocite differentiation and adipogenesis in 3T3-L1 preadipocites were investigated. Treatment with STME in the concentration range of 0-200 μg/ml significantly inhibited the differentiation of 3T3-L1 preadipocites in a dose-dependent manner, as determined by a decrease in intracellular lipid droplets and lipid contents measured by Oil Red O staining. In association with the inhibitory effect of lipid accumulation, the expressions of the proteins concerned with adipogenesis in 3T3-L1 preadipocites were also investigated. Treatment with STME reduced the expressions of peroxisome proliferator-activated receptor r (PPARr), cytidine-cytidine-adenosine-adenosine-thymine (CCAAT)/enhancer-binding proteins α and β (C/EBPα and C/EBPβ) and sterol regulatory element binding protein (SREBP), which are adipocyte specific markers. In flow cytometry analysis, the inhibitory effect of differentiation was caused by G1 arrest and following mitotic clonal expansion cease. Therefore, we also investigated the alteration of G1 phase arrest-related proteins. As a result, the expression of p21 protein was significantly increased, while the expressions of Cdk2, E2F-1 and phospho-Rb were reduced in a dose-dependent manner in STME treated 3T3-L1 cells. According to these results, STME might inhibit differentiation through G1 arrest in 3T3-L1 preadipocytes adipogenesis, and further studies, which are in progress, have to be completed to identify the active compounds.
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KEYWORD
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Sophora tonkinensis Gapnep., adipocyte differentiation, adipocyte specific marker, mitotic clonal expansion, G1 arrest
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