机构：[1]West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China[2]Departmentof Medical Oncology, Sichuan Cancer Hospital & Institute, School of Medicine, University of Electronic Science andTechnology of China, Chengdu, Sichuan, China四川省肿瘤医院[3]Department of Radiation Oncology, Sichuan Cancer Hospital & Institute,Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan,China四川省人民医院四川省肿瘤医院[4]Department of Radiological Protection, Radiation Oncology Key Laboratory of Sichuan Province, Chengdu, Sichuan,China[5]Department of Gastroenterology, The Second Affiliated Hospital of Chengdu Medical College, China National NuclearCorporation 416 Hospital, Chengdu, Sichuan, China[6]State Key Laboratory of Medicinal Chemical Biology, Nankai University,Tianjin, China
Background and Aims: Lipid accumulation is the major characteristic of non-alcoholic fatty liver disease, the prevalence of which continues to rise. We aimed to investigate the effects and mechanisms of icaritin on lipid accumulation. Methods: Cells were treated with icaritin at 0.7, 2.2, 6.7, or 20 mu M for 24 h. The effects on lipid accumulation in L02 and Huh-7 cells were detected by Bodipy and oil red O staining, respectively. Mitochondria biogenesis of L02 cells was detected by MitoTracker Orange staining. Glucose uptake and adenosine triphosphate content of 3T3-L1 adipocytes and C2C12 myotubes were detected. The expression levels of proteins in the adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling pathway, biomarkers of autophagy, and mitochondria biogenesis were measured by western blotting. LC3 puncta were detected by immunofluorescence. Results: Icaritin significantly attenuated lipid accumulation in L02 and Huh-7 cells and boosted the mitochondria biogenesis of L02 cells. Icaritin enhanced glucose uptake, decreased adenosine triphosphate content, and activated the AMPK signaling pathway in 3T3-L1 adipocytes and C2C12 myotubes. Icaritin boosted autophagy and also enhanced the initiation of autophagic flux in 3T3-L1 preadipocytes and C2C12 myoblasts. However, icaritin decreased autophagy and promoted mitochondria biogenesis in 3T3-L1 adipocytes and C2C12 myotubes. Conclusions: Icaritin attenuates lipid accumulation by increasing energy expenditure and regulating autophagy by activating the AMPK pathway.
基金：
National Natural
Science Foundation of China (Grant No. 81770580) and
open funding from the Sichuan Provincial Key Laboratory of
Radiation Oncology (Grant No. 2020FSZLX-02).
第一作者机构：[1]West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China
共同第一作者：
通讯作者：
通讯机构：[1]West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China[5]Department of Gastroenterology, The Second Affiliated Hospital of Chengdu Medical College, China National NuclearCorporation 416 Hospital, Chengdu, Sichuan, China[6]State Key Laboratory of Medicinal Chemical Biology, Nankai University,Tianjin, China[*1]West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, China.
推荐引用方式(GB/T 7714)：
Wu Yue,Yang Ying,Li Fang,et al.Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK[J].JOURNAL OF CLINICAL AND TRANSLATIONAL HEPATOLOGY.2021,9(3):373-383.doi:10.14218/JCTH.2021.00050.
APA：
Wu, Yue,Yang, Ying,Li, Fang,Zou, Jie,Wang, Yu-Hao...&Sun, Xiao-Dong.(2021).Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK.JOURNAL OF CLINICAL AND TRANSLATIONAL HEPATOLOGY,9,(3)
MLA：
Wu, Yue,et al."Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK".JOURNAL OF CLINICAL AND TRANSLATIONAL HEPATOLOGY 9..3(2021):373-383
