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三七皂苷Fe可抑制饮食诱导的肥胖并激活下丘脑室旁核神经元。

Notoginsenoside Fe suppresses diet induced obesity and activates paraventricular hypothalamic neurons.

作者信息

Li Hongli, Liu Yalei, Liu Chuhe, Luo Lingling, Yao Yin, Li Fei, Yin Liufang, Xu Lai, Tong Qingchun, Huang Cheng, Fan Shengjie

机构信息

Drug Discovery Laboratory, School of Pharmacy, Shanghai University of Traditional Chinese Medicine Shanghai 201203 China

Brown Foundation Institute of Molecular Medicine and Program in Neuroscience, Graduate School of Biological Sciences, University of Texas McGovern Medical School Houston TX USA.

出版信息

RSC Adv. 2019 Jan 11;9(3):1290-1298. doi: 10.1039/c8ra07842d. eCollection 2019 Jan 9.

DOI:10.1039/c8ra07842d
PMID:35518019
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9059641/
Abstract

Obesity has become a major public health challenge worldwide. Energy imbalance between calorie acquisition and consumption is the fundamental cause of obesity. Notoginsenoside Fe is a naturally occurring compound in , a herb used in the treatment of cardiovascular diseases in traditional Chinese medicine. Here, we evaluated the effect of notoginsenoside Fe on obesity development induced by high-fat diet in C57BL/6 mice. Our results demonstrated that notoginsenoside Fe decreased food intake and body weight, as well as protected liver structure integrity and normal function. Metabolic cage analysis showed that notoginsenoside Fe also promoted resting metabolic rate. In addition, intracerebroventricular (i.c.v) injection of notoginsenoside Fe induced C-Fos expression in the paraventricular nucleus (PVH) but not the arcuate nucleus (ARC) of the hypothalamus. These results suggest that Fe may reduce body weight through the activation of energy-sensing neurons in the hypothalamus.

摘要

肥胖已成为全球主要的公共卫生挑战。热量摄入与消耗之间的能量失衡是肥胖的根本原因。三七皂苷Fe是中药中用于治疗心血管疾病的草药三七中的一种天然化合物。在此,我们评估了三七皂苷Fe对高脂饮食诱导的C57BL/6小鼠肥胖发展的影响。我们的结果表明,三七皂苷Fe减少了食物摄入量和体重,并保护了肝脏结构完整性和正常功能。代谢笼分析表明,三七皂苷Fe还提高了静息代谢率。此外,脑室内注射三七皂苷Fe诱导下丘脑室旁核(PVH)而非弓状核(ARC)中的C-Fos表达。这些结果表明,三七皂苷Fe可能通过激活下丘脑的能量感应神经元来减轻体重。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e436/9059641/22cf9e245006/c8ra07842d-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e436/9059641/e0ac6c8757a8/c8ra07842d-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e436/9059641/fa171539ecb4/c8ra07842d-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e436/9059641/680e45b62ea1/c8ra07842d-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e436/9059641/797e715af16c/c8ra07842d-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e436/9059641/22cf9e245006/c8ra07842d-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e436/9059641/e0ac6c8757a8/c8ra07842d-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e436/9059641/fa171539ecb4/c8ra07842d-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e436/9059641/680e45b62ea1/c8ra07842d-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e436/9059641/797e715af16c/c8ra07842d-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e436/9059641/22cf9e245006/c8ra07842d-f5.jpg

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