Isoliquiritigenin attenuates non-alcoholic fatty liver disease via the amelioration of hepatic inflammation and autophagy in mice

被引:5
|
作者
Jian, Lina [1 ,2 ,3 ]
Wu, Huixing [3 ]
Zeng, Haiyan [4 ]
Quan, Ting [5 ]
Xia, Fan [1 ,2 ]
Xiang, Shijian [1 ,2 ]
Zhou, Benjie [1 ,2 ]
机构
[1] Sun Yat Sen Univ, Dept Pharm, Affiliated Hosp 7, Shenzhen 518107, Peoples R China
[2] Shenzhen Key Lab Chinese Med Act Subst Screening &, Shenzhen 518107, Peoples R China
[3] Guangdong Med Univ, Sch Pharm, Dongguan 523808, Peoples R China
[4] Univ Chinese Acad Sci, Shenzhen Hosp, Clin Lab, Shenzhen 518106, Peoples R China
[5] Hubei Univ Med, Taihe Hosp, Dept Pharm, Shiyan 442000, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
Isoliquiritigenin; Autophagy; NAFLD; PI3K/AKT/mTOR; Inflammation; PI3K/AKT/MTOR PATHWAY; ACTIVATION; MECHANISMS; 3-METHYLADENINE; INHIBITION; STEATOSIS;
D O I
10.1016/j.jff.2023.105770
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
The therapeutic and pharmacological potential of isoliquiritigenin has been reported in relieving inflammation and lipid metabolism disorders, particularly in the context of non-alcoholic fatty liver disease (NAFLD). The aim of this study is to investigate the effects of isoliquiritigenin on NAFLD, obesity-associated metabolic symptoms in vivo and in vitro, and explore new mechanisms underlying its effects. Our study revealed that isoliquiritigenin effectively reduced lipid accumulation and suppressed inflammation factors expression in hepatocytes and high fat diet (HFD) mice. Additionally, it prevented body weight gain and liver damage in HFD mice. Importantly, RNA-sequencing results revealed that isoliquiritigenin exerts its anti-NAFLD effect may through the mTOR pathway and autophagy. Rescue experiments further confirmed that it inhibits inflammation by suppressing the PI3K/AKT/mTOR pathway and reduces lipid accumulation by promoting autophagy. Therefore, it holds promise as a novel treatment for NAFLD.
引用
收藏
页数:13
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