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(L.)Pers.提取物通过激活AMP依赖的激酶信号通路抑制3T3-L1细胞中活性氧(ROS)的产生和脂肪积累。

(L.) Pers. Extract Inhibits Reactive Oxygen Species (ROS) Production and Fat Accumulation in 3T3-L1 Cells by Activating an AMP-Dependent Kinase Signaling Pathway.

作者信息

Choi Yoon-Hee, Lee Ok-Hwan, Zheng Yulong, Kang Il-Jun

机构信息

Department of Food and Nutrition, Hallym Polytechnic University, Chuncheon 24210, Korea.

Department of Food Science and Biotechnology, Kangwon National University, Chuncheon 24341, Korea.

出版信息

Antioxidants (Basel). 2019 May 20;8(5):139. doi: 10.3390/antiox8050139.

Abstract

Obesity is one of the major public health problems in the world because it is implicated in metabolic syndromes, such as type 2 diabetes, hypertension, and cardiovascular diseases. The objective of this study was to investigate whether (L.) Pers. (EAP) extract suppresses reactive oxygen species (ROS) production and fat accumulation in 3T3-L1 cells by activating an AMP-dependent kinase (AMPK) signaling pathway. Our results showed that EAP water extract significantly inhibits ROS production, adipogenesis, and lipogenesis during differentiation of 3T3-L1 preadipocytes. In addition, EAP decreased mRNA and protein levels of proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα). Moreover, EAP suppressed mRNA expressions of fatty acid synthase (FAS), lipoprotein lipase (LPL), adipocyte protein 2 (aP2) in a dose-dependent manner. Whereas, EAP upregulated adiponectin expression, phosphorylation levels of AMPK and carnitine palmitoyltransferase 1 (CPT-1) protein level during differentiation of 3T3-L1 preadipocytes. These results suggest that EAP water extract can exert ROS-linked anti-obesity effect through the mechanism that might involve inhibition of ROS production, adipogenesis and lipogenesis via an activating AMPK signaling pathway.

摘要

肥胖是全球主要的公共卫生问题之一,因为它与代谢综合征有关,如2型糖尿病、高血压和心血管疾病。本研究的目的是调查佩兰(Eupatorium fortunei Turcz.)提取物是否通过激活AMP依赖激酶(AMPK)信号通路来抑制3T3-L1细胞中活性氧(ROS)的产生和脂肪积累。我们的结果表明,佩兰水提取物在3T3-L1前脂肪细胞分化过程中显著抑制ROS的产生、脂肪生成和脂质生成。此外,佩兰降低了增殖激活受体γ(PPARγ)和CCAAT/增强子结合蛋白α(C/EBPα)的mRNA和蛋白质水平。而且,佩兰以剂量依赖的方式抑制脂肪酸合酶(FAS)、脂蛋白脂肪酶(LPL)、脂肪细胞蛋白2(aP2)的mRNA表达。然而,在3T3-L1前脂肪细胞分化过程中,佩兰上调了脂联素的表达、AMPK的磷酸化水平以及肉碱棕榈酰转移酶1(CPT-1)的蛋白水平。这些结果表明,佩兰水提取物可通过激活AMPK信号通路抑制ROS产生、脂肪生成和脂质生成的机制发挥与ROS相关的抗肥胖作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d549/6562390/cd252b4995cb/antioxidants-08-00139-g001.jpg

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