Phytomedicine ( IF 6.7 ) Pub Date : 2019-07-20 , DOI: 10.1016/j.phymed.2019.153038 Jihang Chen 1 , Pou Kuan Leong 2 , Hoi Yan Leung 2 , Wing Man Chan 2 , Hoi Shan Wong 3 , Kam Ming Ko 2
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Background
HCY2, a triterpenoid-enriched extract of Cynomorii Herba, has been shown to reduce body weight and adiposity and attenuate manifestations of the associated metabolic syndrome in high-fat-diet (HFD)-fed mice.
Purpose
The current study aimed to investigate the biochemical mechanism underlying the anti-obesity effect produced by HCY2.
Study design
An HCY2-containing extract was examined for its effects on the regulation of adenosine monophosphate-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma co-activator-1 (PGC1) pathways and the protein expression related to mitochondrial uncoupling and biogenesis in skeletal muscle using an HFD-induced obese mouse model.
Methods
The obese mouse model was produced by providing HFD (60% kcal from fat) ad libitum. The effects and signaling mechanisms of HCY2 were examined using analytical procedures which included enzyme-linked immunosorbent assay kits, Western blot analysis, and the use of a Clark-type oxygen electrode.
Results
The current study revealed that the weight reduction produced by HCY2 is associated with the activation of the AMPK signaling pathway, with resultant increases in mitochondrial biogenesis and expression of uncoupling protein 3 in skeletal muscle in vivo. The use of a recoupler, ketocholestanol, delineated the precise role of mitochondrial uncoupling in the anti-obesity effect afforded by HCY2 in obese mice.
Conclusion
Our experimental findings offer a promising prospect for the use of HCY2 in the management of obesity through the regulation of AMPK/PGC1 pathways.
中文翻译：
48富含三萜类的锁阳提取物对高脂饮食诱导的肥胖小鼠的抗肥胖作用的生化机制。
背景
HCY2是富含三萜类的Cynomorii Herba提取物，已显示可减轻高脂饮食（HFD）喂养的小鼠的体重和肥胖，并减轻相关代谢综合征的表现。
目的
目前的研究旨在研究由HCY2产生的抗肥胖作用的生化机制。
学习规划
检查了含有HCY2的提取物对单磷酸腺苷活化蛋白激酶（AMPK）/过氧化物酶体增殖物活化受体γco-activator-1（PGC1）通路的调节作用以及与线粒体解偶联和生物发生有关的蛋白质表达骨骼肌使用HFD诱导的肥胖小鼠模型。
方法
肥胖小鼠模型是通过随意提供HFD（脂肪中的大卡含量为60％）产生的。使用包括酶联免疫吸附测定试剂盒，蛋白质印迹分析和Clark型氧电极在内的分析程序检查了HCY2的作用和信号传导机制。
结果
当前的研究表明，HCY2产生的体重减轻与AMPK信号通路的激活有关，从而导致体内骨骼肌线粒体生物发生的增加和解偶联蛋白3的表达增加。使用偶联剂酮胆固醇描述了线粒体解偶联在肥胖小鼠中由HCY2提供的抗肥胖作用中的确切作用。
结论
我们的实验结果为通过调节AMPK / PGC1途径在肥胖管理中使用HCY2提供了有希望的前景。
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