甾醇调节元件结合蛋白
mTORC1型
非酒精性脂肪肝
内科学
内分泌学
脂肪肝
脂质代谢
胰岛素抵抗
下调和上调
体内
化学
生物化学
胆固醇
生物
胰岛素
疾病
医学
信号转导
甾醇
PI3K/AKT/mTOR通路
生物技术
基因
作者
Huazhen Liu,Yonger Chen,Yifan Wen,Shumin Zhu,Song Huang,Lian He,Shaozhen Hou,Xiaoping Lai,Shuxian Chen,Zhenhua Dai,Jian Liang
标识
DOI:10.1021/acs.jafc.1c01645
摘要
We aimed to investigate whether phloridzin could alleviate nonalcoholic fatty liver disease (NAFLD) in mice, which was induced by feeding a high-fat diet (HFD). We initially analyzed the effect of phloridzin on alleviating HFD-induced NAFLD in C57BL/6J mice and oleic acid (OA)-stimulated human normal liver L-02 cells (L02). Then, we investigated the mechanism of phloridzin on the mTORC1/sterol-regulatory element-binding protein-1c (SREBP-1c) signaling pathway by siRNA analysis, qRT-PCR, flow cytometry, and western blot analysis in vivo and in vitro. The results revealed that phloridzin significantly inhibited the increase in body weight, alleviated abnormal lipid metabolism, and decreased lipid biosynthesis and insulin resistance. Moreover, phloridzin augmented the number of CD8+CD122+PD-1+ Tregs and CD4+FoxP3+ Tregs in HFD-fed C57BL/6J mice and HFD-fed aP2-SREBF1c mice and downregulated the mTORC1/SREBP-1c signaling pathway-related protein expressions in vivo and in vitro. Furthermore, phloridzin reduced the expression of SREBP-1c in SREBP-1c-RNAi-lentivirus-transfected L02 cells and reversed the SREBP-1c expression in HFD-fed aP2-SREBF1c transgenic mice. Phloridzin ameliorates lipid accumulation and insulin resistance via inhibiting the mTORC1/SREBP-1c pathways. These results indicated that phloridzin may actively ameliorate NAFLD.
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