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红芪多糖通过激活腺苷酸活化蛋白激酶途径抑制非酒精性脂肪性肝病大鼠模型的脂质代谢功能障碍。

Radix Hedysari polysaccharide suppresses lipid metabolism dysfunction in a rat model of non‑alcoholic fatty liver disease via adenosine monophosphate‑activated protein kinase pathway activation.

作者信息

Sun Wei-Ming, Wang Yu-Ping, Duan Yong-Qiang, Shang Hong-Xia, Cheng Wei-Dong

机构信息

Institute of Integrated Chinese and Western Medicine, School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.

Key Laboratory for Gastrointestinal Diseases of Gansu Province, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.

出版信息

Mol Med Rep. 2014 Sep;10(3):1237-44. doi: 10.3892/mmr.2014.2327. Epub 2014 Jun 13.

DOI:10.3892/mmr.2014.2327
PMID:24927063
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4121409/
Abstract

Oxidative stress and excess hepatic lipid accumulation contribute to non‑alcoholic fatty liver disease. Radix Hedysari polysaccharides (RHP) have attracted interest due to their antioxidant properties and immunomodulatory effects. However, the effect of RHP on hepatic lipid metabolism remains to be elucidated. In the present study, the response of Sprague‑Dawley rat livers to a high‑fat diet and RHP treatment was investigated by evaluating body weight, liver histology, hepatic lipid content, adenosine monophosphate‑activated protein kinase (AMPK) activity and lipid metabolism gene transcriptional profiles. The present study demonstrated that RHP ameliorated lipid metabolism disorders, regulated hepatic lipid content, improved liver inflammation and damage, activated AMPK via phosphorylation, upregulated peroxisome proliferator‑activated receptor α and downregulated the mRNA expression of sterol regulatory element binding protein‑1c in rat livers, which reduced lipogenesis and increased lipolysis. Taken together, these results suggested that RHP effectively ameliorates lipid metabolism disorders in rat livers; thus, RHP may be a potential therapeutic agent in the prevention of hepatic steatosis.

摘要

氧化应激和肝脏脂质过度积累会导致非酒精性脂肪性肝病。红芪多糖(RHP)因其抗氧化特性和免疫调节作用而受到关注。然而,RHP对肝脏脂质代谢的影响仍有待阐明。在本研究中,通过评估体重、肝脏组织学、肝脏脂质含量、腺苷单磷酸激活蛋白激酶(AMPK)活性和脂质代谢基因转录谱,研究了Sprague-Dawley大鼠肝脏对高脂饮食和RHP处理的反应。本研究表明,RHP改善了脂质代谢紊乱,调节了肝脏脂质含量,改善了肝脏炎症和损伤,通过磷酸化激活了AMPK,上调了过氧化物酶体增殖物激活受体α,并下调了大鼠肝脏中固醇调节元件结合蛋白-1c的mRNA表达,从而减少了脂肪生成并增加了脂肪分解。综上所述,这些结果表明RHP能有效改善大鼠肝脏的脂质代谢紊乱;因此,RHP可能是预防肝脂肪变性的潜在治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b74/4121409/b37163d4920f/MMR-10-03-1237-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b74/4121409/7dc91102e275/MMR-10-03-1237-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b74/4121409/91f98961f49a/MMR-10-03-1237-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b74/4121409/da78765dde8e/MMR-10-03-1237-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b74/4121409/b37163d4920f/MMR-10-03-1237-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b74/4121409/7dc91102e275/MMR-10-03-1237-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b74/4121409/91f98961f49a/MMR-10-03-1237-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b74/4121409/da78765dde8e/MMR-10-03-1237-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b74/4121409/b37163d4920f/MMR-10-03-1237-g03.jpg

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