Medium- and long-chain triglyceride propofol activates PI3K/AKT pathway and inhibits non-alcoholic fatty liver disease by inhibiting lipid accumulation

被引：1
|
作者：
Liu, Hui [1 ]
Hao, Mingshuo [2 ]
Liu, Wen [1 ]
Chen, Haiyan [1 ]
Han, Changlong [1 ]
Shao, Yun [1 ]
Wang, Liyuan [1 ]
机构：
[1] Univ Shanghai Sci & Technol, Shidong Hosp, Dept anesthesiol, Shidong Hosp, Shanghai 200438, Peoples R China
[2] Jining 1 Peoples Hosp, Pathol Dept, 13 Jiankang Rd, Jining 272002, Shandong, Peoples R China
来源：
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES | 2024年 / 56卷 / 01期
关键词：
NAFLD; Liver disease; Liver steatosis; MCT/LCT; PI3K/AKT; METABOLISM; INJECTION; PAIN;
D O I：
10.1007/s10863-023-09997-0
中图分类号：
Q6 [生物物理学];
学科分类号：
071011 ;
摘要：
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease. The mechanism by which medium- and long-chain triglyceride (MCT/LCT) propofol plays a role in promoting NAFLD remains unclear. In this study, we investigated the effect of MCT/LCT propofol on NAFLD progression and its mechanism of action. In Huh-7 and HepG3 cells induced by free fatty acids (FFA), propofol downregulated the expression levels of TG and lipid metabolism-related proteins by promoting the activation of the PI3K/AKT pathway and suppressing FFA-induced lipid metabolic disorders. In a high-fat diet (HFD) -induced NAFLD mouse model, we demonstrated that propofol significantly inhibited liver steatosis, inflammatory cell infiltration, and fibrosis. In conclusion, our results suggest that MCT/LCT propofol reduces liver lipid accumulation by activating the PI3K/AKT pathway and further suppressing the NAFLD process.
引用
收藏
页码：45 / 53
页数：9
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