Psoralen Suppresses Lipid Deposition by Alleviating Insulin Resistance and Promoting Autophagy in Oleate-Induced L02 Cells
Yuhao Wang,
Yonglun Wang,
Fang Li,
Jie Zou,
Xiaoqian Li,
Mengxia Xu,
Daojiang Yu,
Yijia Ma,
Wei Huang,
Xiaodong Sun,
Yuanyuan Zhang
Affiliations
Yuhao Wang
West China School of Pharmacy, Sichuan University, Chengdu 610041, China
Yonglun Wang
West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China
Fang Li
Department of Hepatopancreatobiliary Surgery, Sichuan Cancer Hospital and Institute, School of Medicine, University of Electronic Science and Technology of China, Chengdu 610041, China
Jie Zou
West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China
Xiaoqian Li
West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China
Mengxia Xu
West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China
Daojiang Yu
Department of Plastic Surgery, The Second Affiliated Hospital of Chengdu Medical College, China National Nuclear Corporation 416 Hospital, Chengdu 610051, China
Yijia Ma
West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China
Wei Huang
Department of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou 646000, China
Xiaodong Sun
West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China
Yuanyuan Zhang
West China School of Pharmacy, Sichuan University, Chengdu 610041, China
Non-alcoholic fatty liver disease (NAFLD) held a high global prevalence in recent decades. Hepatic lipid deposition is the major characteristic of NAFLD. We aim to explore the mechanisms of psoralen on lipid deposition in NAFLD. The effects of psoralen on insulin resistance, lipid deposition, the expression and membrane translocation of glucose transporter type 4 (GLUT4), autophagy, and lipogenesis enzymes were determined on sodium oleate-induced L02 cells. Chloroquine and 3-MA were employed. The AMP-activated protein kinase alpha (AMPKα) was knocked down by siRNA. Psoralen alleviated insulin resistance in sodium oleate-induced L02 hepatocytes by upregulating the expression and membrane translocation of GLUT4. Psoralen inhibited lipid accumulation by decreasing the expression of key lipogenesis enzymes. Psoralen promotes autophagy and the autophagic flux to enhance lipolysis. Psoralen promoted the fusion of the autophagosome with the lysosome. Both chloroquine and 3-MA blocked the effects of psoralen on autophagy and lipid accumulation. The AMPKα deficiency attenuated the effects of psoralen on autophagy and lipid accumulation. Our study demonstrated that as an antioxidant, psoralen attenuates NAFLD by alleviating insulin resistance and promoting autophagy via AMPK, suggesting psoralen to be a promising candidate for NAFLD.
