Evidence map›Paper›PMID 34221923›Full record

ArticleJournal of clinical and translational hepatology2021

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

Yue Wu, Ying Yang, Fang Li, Jie Zou, Yu-Hao Wang, Meng-Xia Xu, Yong-Lun Wang, Rui-Xi Li, Yu-Ting Sun, Shun Lu and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Journal of clinical and translational hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 12 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Yue WuWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Ying YangWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Fang LiDepartment of Medical Oncology, Sichuan Cancer Hospital & Institute, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Jie ZouWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Yu-Hao WangWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Meng-Xia XuWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Yong-Lun WangWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Rui-Xi LiWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Yu-Ting SunWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Shun LuDepartment of Radiation Oncology, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Yuan-Yuan ZhangWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.ORCID 0000-0002-9263-6262
Xiao-Dong SunWest China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.ORCID 0000-0002-7062-8931
West China Medical Center of Sichuan University · CNUniversity of Electronic Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsLipid 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.

methodsCells 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.

resultsIcaritin 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.

conclusionsIcaritin attenuates lipid accumulation by increasing energy expenditure and regulating autophagy by activating the AMPK pathway.

Indexed as

AMPKAutophagyIcaritinLipid accumulationNAFLD

Identifiers

PMID34221923
PMCPMC8237137
OpenAlexW3135477858

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.