Liu Bo, Tang Yuan, Song Zhenyan, Ge Jinwen
College of Integrated Traditional Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, Hunan 410208, P.R. China.
Mol Med Rep. 2021 Jul;24(1). doi: 10.3892/mmr.2021.12140. Epub 2021 May 13.
The present study sought to elucidate the role of polysaccharide (PSP) in high‑fat diet (HFD)‑induced mouse obesity and investigated the primary molecular mechanism underlaying these effects. An obese mouse model was established by feeding HFD and three doses of PSP were administered intragastrically. Changes in body weight, serum lipids and parameters were recorded and the mechanism was explored by reverse transcription‑quantitative PCR and western blotting. Body weight, blood lipids, blood glucose, insulin, resistin, adiponectin, liver weight and abdominal fat pads weight were reduced by PSP and abnormal expression levels of inflammatory factors such as TNF‑α, IL‑6, IL‑1β and iNOS and lipid metabolism genes such as FAS, SREBP‑1, PPARα and CPT‑1were also reversed by PSP. The 5' adenosine monophosphate‑activated protein kinase (AMPK) signaling pathway was activated in PSP mouse liver, leading to lipid‑lowering and anti‑inflammatory effects. The results therefore suggested that PSP exhibited lipid‑lowering and anti‑inflammatory effects by activating the AMPK signaling pathway.
本研究旨在阐明多糖(PSP)在高脂饮食(HFD)诱导的小鼠肥胖中的作用,并探讨其作用的主要分子机制。通过喂食高脂饮食建立肥胖小鼠模型,并通过胃内给予三种剂量的PSP。记录体重、血脂和相关参数的变化,并通过逆转录定量PCR和蛋白质免疫印迹法探索其机制。PSP可降低体重、血脂、血糖、胰岛素、抵抗素、脂联素、肝脏重量和腹部脂肪垫重量,还可逆转TNF-α、IL-6、IL-1β和诱导型一氧化氮合酶等炎症因子以及脂肪酸合酶、固醇调节元件结合蛋白-1、过氧化物酶体增殖物激活受体α和肉碱/有机阳离子转运体-1等脂质代谢基因的异常表达水平。PSP可激活小鼠肝脏中的5'-腺苷单磷酸激活蛋白激酶(AMPK)信号通路,从而产生降脂和抗炎作用。因此,结果表明PSP通过激活AMPK信号通路发挥降脂和抗炎作用。