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牛蒡子苷元通过诱导AMPK激活抑制脂肪生成并减轻高脂饮食诱导的肥胖小鼠的体重增加。

Arctigenin Inhibits Adipogenesis by Inducing AMPK Activation and Reduces Weight Gain in High-Fat Diet-Induced Obese Mice.

作者信息

Han Yo-Han, Kee Ji-Ye, Park Jinbong, Kim Hye-Lin, Jeong Mi-Young, Kim Dae-Seung, Jeon Yong-Deok, Jung Yunu, Youn Dong-Hyun, Kang JongWook, So Hong-Seob, Park Raekil, Lee Jong-Hyun, Shin Soyoung, Kim Su-Jin, Um Jae-Young, Hong Seung-Heon

机构信息

Department of Oriental Pharmacy, Wonkwang-Oriental Medicines Research Institute, College of Pharmacy, Wonkwang University, 460 Iksandae-ro, Iksan, Jeonbuk, 54538, Republic of Korea.

Department of Pharmacology, Institute of Korean Medicine, College of Korean Medicine, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul, 02447, Republic of Korea.

出版信息

J Cell Biochem. 2016 Sep;117(9):2067-77. doi: 10.1002/jcb.25509. Epub 2016 May 26.

Abstract

Although arctigenin (ARC) has been reported to have some pharmacological effects such as anti-inflammation, anti-cancer, and antioxidant, there have been no reports on the anti-obesity effect of ARC. The aim of this study is to investigate whether ARC has an anti-obesity effect and mediates the AMP-activated protein kinase (AMPK) pathway. We investigated the anti-adipogenic effect of ARC using 3T3-L1 pre-adipocytes and human adipose tissue-derived mesenchymal stem cells (hAMSCs). In high-fat diet (HFD)-induced obese mice, whether ARC can inhibit weight gain was investigated. We found that ARC reduced weight gain, fat pad weight, and triglycerides in HFD-induced obese mice. ARC also inhibited the expression of peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα) in in vitro and in vivo. Furthermore, ARC induced the AMPK activation resulting in down-modulation of adipogenesis-related factors including PPARγ, C/EBPα, fatty acid synthase, adipocyte fatty acid-binding protein, and lipoprotein lipase. This study demonstrates that ARC can reduce key adipogenic factors by activating the AMPK in vitro and in vivo and suggests a therapeutic implication of ARC for obesity treatment. J. Cell. Biochem. 117: 2067-2077, 2016. © 2016 Wiley Periodicals, Inc.

摘要

尽管牛蒡子苷元(ARC)已被报道具有抗炎、抗癌和抗氧化等药理作用,但关于ARC的抗肥胖作用尚无报道。本研究的目的是探讨ARC是否具有抗肥胖作用并介导AMP激活的蛋白激酶(AMPK)途径。我们使用3T3-L1前脂肪细胞和人脂肪组织来源的间充质干细胞(hAMSCs)研究了ARC的抗脂肪生成作用。在高脂饮食(HFD)诱导的肥胖小鼠中,研究了ARC是否能抑制体重增加。我们发现ARC减少了HFD诱导的肥胖小鼠的体重增加、脂肪垫重量和甘油三酯。ARC在体外和体内还抑制了过氧化物酶体增殖物激活受体γ(PPARγ)和CCAAT/增强子结合蛋白α(C/EBPα)的表达。此外,ARC诱导AMPK激活,导致包括PPARγ、C/EBPα、脂肪酸合酶、脂肪细胞脂肪酸结合蛋白和脂蛋白脂肪酶在内的脂肪生成相关因子的下调。本研究表明,ARC在体外和体内均可通过激活AMPK来降低关键脂肪生成因子的水平,并提示ARC在肥胖治疗中的潜在治疗意义。《细胞生物化学杂志》117: 2067 - 2077, 2016。© 2016威利期刊公司。

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