BACKGROUND Although rubrofusarin-6-β-gentiobioside (RFG), which is a component of Cassiae tora seed, could likely regulate hyperlipidemia, its anti-obesity effect and related mechanism have not been elucidated. PURPOSE The aim of this study was to examine whether RFG can ameliorate obesity and the mechanism of lipid accumulation regulated by RFG. STUDY DESIGN In in vitro experiments, we confirmed the anti-adipogenic effect of RFG using 3T3-L1 cells and human adipose mesenchymal stem cells (hAMSCs). To confirm the anti-obesity effect, High-Fat Diet (HFD)-induced obese mice were selected as a model. METHODS We investigated anti-adipogenic effects of RFG using MTS assay, Oil Red O Staining, real-time RT-PCR, western blot analysis, and immunofluorescence staining. The anti-obesity effect of RFG was confirmed in HFD-induced mice model using hematoxylin and eosin staining and serum analysis. RESULTS RFG inhibited lipid accumulation in 3T3-L1 cells and hAMSCs by reducing expression of mammalian targets of rapamycin (mTOR), peroxisome proliferator-activated receptor (PPAR)γ, and CCAAT-enhancer binding protein (C/EBP)α. RFG phosphorylated AMP-activated protein kinase (AMPK) in a liver kinase B (LKB) 1-independent manner. Moreover, the anti-adipogenic effect of RFG was blocked by AMPK inhibitor. These results suggest that RFG inhibits lipid accumulation via AMPK signaling. Furthermore, RFG reduced the body weight, size of epididymal white adipose tissue (eWAT), and fatty liver in the mice. RFG also suppressed levels of adipogenic factors PPARγ, C/EBPα, FAS, LPL, and aP2) by activating AMPK in the eWAT and liver. CONCLUSION RFG can ameliorate obesity, and thus, could be used as a therapeutic agent for treating obesity.

中文翻译：

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芸苔红素-6-β-龙胆生物苷可通过调节AMPK / mTOR信号传导来抑制脂质蓄积和体重增加。

背景技术虽然决明子种子中的红果素6-β-龙胆二糖苷（RFG）可能可以调节高脂血症，但其抗肥胖作用及其相关机理尚未阐明。目的本研究的目的是研究RFG是否可以改善肥胖症以及RFG调节脂质蓄积的机制。研究设计在体外实验中，我们证实了使用3T3-L1细胞和人脂肪间充质干细胞（hAMSC）抑制RFG的抗脂肪形成作用。为了证实抗肥胖作用，选择高脂饮食（HFD）诱导的肥胖小鼠作为模型。方法我们使用MTS分析，油红O染色，实时RT-PCR，western印迹分析和免疫荧光染色研究了RFG的抗脂肪形成作用。使用苏木精和曙红染色和血清分析在HFD诱导的小鼠模型中证实了RFG的抗肥胖作用。结果RFG通过降低哺乳动物雷帕霉素（mTOR），过氧化物酶体增殖物激活受体（PPAR）γ和CCAAT增强子结合蛋白（C / EBP）α的表达来抑制3T3-L1细胞和hAMSC中脂质的积累。RFG以肝激酶B（LKB）1独立的方式磷酸化AMP激活的蛋白激酶（AMPK）。此外，RFG的抗脂肪形成作用被AMPK抑制剂阻断。这些结果表明，RFG通过AMPK信号传导抑制脂质蓄积。此外，RFG减轻了小鼠的体重，附睾白色脂肪组织（eWAT）的大小和脂肪肝。RFG还通过激活eWAT和肝脏中的AMPK抑制脂肪生成因子PPARγ，C /EBPα，FAS，LPL和aP2的水平。