Journal of Clinical and Translational Hepatology

Journal of Clinical and Translational Hepatology

Thursday, 12 / 09 / 2021

Abstract

ORIGINAL ARTICLE

Icaritin Attenuates Lipid Accumulation by Increasing Energy Expenditure and Autophagy Regulated by Phosphorylating AMPK

Yue Wu1,#, Ying Yang1,#, Fang Li2,#, Jie Zou1, Yu-Hao Wang1, Meng-Xia Xu1, Yong-Lun Wang1, Rui-Xi Li1, Yu-Ting Sun1, Shun Lu3,4, Yuan-Yuan Zhang1,5,* and Xiao-Dong Sun1,6,*

1  West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China
2  Department of Medical Oncology, Sichuan Cancer Hospital & Institute, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China
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
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 Nuclear Corporation 416 Hospital, Chengdu, Sichuan, China
6  State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China
#Contributed equally to this work.
*Correspondence to: Yuan-Yuan Zhang, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, China. ORCID:  http://orcid.org/0000-0002-9263-6262 . Tel: +86-28-8550-1278, Fax: +86-28-8550-1278, E-mail: This email address is being protected from spambots. You need JavaScript enabled to view it. , This email address is being protected from spambots. You need JavaScript enabled to view it. ; Xiao-Dong Sun, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, China. ORCID:http://orcid.org/0000-0002-7062-8931 . Tel: +86-28-8550-1278, Fax: +86-28-8550-1278, E-mail: This email address is being protected from spambots. You need JavaScript enabled to view it.

Journal of Clinical and Translational Hepatology 2021;9(3):373-383 DOI: 10.14218/JCTH.2021.00050
Received: February 3, 2021 Accepted: March 4, 2021 Published online: March 8, 2021

Abstract

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 µM 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.

Keywords

Icaritin, Lipid accumulation, NAFLD, AMPK, Autophagy

Journal of Clinical and Translational Hepatology 2021 vol. 9, 373-383  [ Html  ] [ PDF Full-text ]

© 2021 Authors. This is an Open Access article distributed under the terms of the  Creative Commons Attribution-Noncommercial 4.0 License(CC BY-NC 4.0), permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

 

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