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黄芩素通过调节早期脂肪生成和m-TOR信号传导来抑制脂质积累。

Baicalein inhibits lipid accumulation by regulating early adipogenesis and m-TOR signaling.

作者信息

Seo Min-Jung, Choi Hyeon-Son, Jeon Hui-Jeon, Woo Mi-Seon, Lee Boo-Yong

机构信息

Department of Food Science and Biotechnology, CHA University, Kyonggi 463-836, South Korea.

Department of Food Science and Biotechnology, CHA University, Kyonggi 463-836, South Korea.

出版信息

Food Chem Toxicol. 2014 May;67:57-64. doi: 10.1016/j.fct.2014.02.009. Epub 2014 Feb 19.

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 p70S6K. 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.

摘要

黄芩素是一种源自黄芩的黄酮类化合物。在本研究中,我们研究了黄芩素如何抑制3T3-L1细胞脂肪生成过程中的脂质积累。我们的数据表明,黄芩素以剂量依赖性方式抑制脂肪生成过程中的脂质积累。黄芩素的抑制作用仅限于脂肪生成早期阶段。细胞周期分析表明,黄芩素通过下调细胞周期蛋白诱导细胞周期停滞在G0/G1期。此外,黄芩素抑制早期脂肪生成因子的mRNA表达,导致晚期脂肪生成因子在mRNA和蛋白质水平下调。黄芩素对脂肪生成因子的抑制作用与脂质合成酶的下调相关。此外,黄芩素负调控脂肪生成过程中参与脂质积累的m-TOR信号通路,从而抑制m-TOR和p70S6K的磷酸化。在一项斑马鱼研究中,黄芩素显著减少尼罗红染色中的脂质积累。与使用细胞系的报告一致,黄芩素以剂量依赖性方式降低脂肪生成因子的mRNA表达。该结果反映了基于甘油三酯测定的总甘油三酯水平的降低。我们的数据表明,黄芩素通过控制3T3-L1细胞的细胞周期和m-TOR信号来抑制脂质积累,并且在斑马鱼模型中发现了其抗脂肪生成作用。

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