Evidence map›Paper›PMID 40165660›Full record

ArticleHistology and histopathology2025

Licochalcone A ameliorates lipid accumulation in metabolic dysfunction-associated steatotic liver disease via upregulating PPARα/CPT1α.

Wenrui Zhu, Hongfeng Xu, Rui Yan, Luqi Qiu, Guojun Wang, Yantao Zhu

Abstract read
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In one paragraph

Article in Histology and histopathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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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

1 citing paper in PubMed.

  1. Review
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

6 authors.

Wenrui ZhuDepartment of Traditional Chinese Medicine, Shaoxing Hospital of Traditional Chinese Medicine Affiliated to Zhejiang Chinese Medical University, Shaoxing, China.
Hongfeng XuDepartment of Clinical Pharmacy, Shaoxing Hospital of Traditional Chinese Medicine Affiliated to Zhejiang Chinese Medical University, Shaoxing, China.
Rui YanDepartment of Traditional Chinese Medicine, Shaoxing Hospital of Traditional Chinese Medicine Affiliated to Zhejiang Chinese Medical University, Shaoxing, China.
Luqi QiuDepartment of Traditional Chinese Medicine Pharmacy, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
Guojun Wang *Jinhua TCM Hospital Affiliated to Zhejiang Chinese Medical University, Jinhua, China. wang1223505@163.com.
Yantao Zhu *Jinhua TCM Hospital Affiliated to Zhejiang Chinese Medical University, Jinhua, China. zhuyantao299@126.com.

Funding

Jinhua City Science and Technology Plan Project 2022-3-113Zhejiang Province Traditional Chinese Medicine Science and Technology Project 2023ZF174Zhejiang Province Traditional Chinese Medicine Science and Technology Project 2023ZL726Zhejiang Province Traditional Chinese Medicine Science and Technology Project 2023ZL728Zhejiang Province Traditional Chinese Medicine Science and Technology Project 2023ZR033
6 · The paper itself

Abstract

backgroundMetabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent hepatic disorder with high morbidity and mortality. Licochalcone A (LiA) exhibits significant therapeutic efficacy in obesity through diverse pharmacological mechanisms. This study aimed to explore the efficacy and underlying mechanism of LiA in attenuating MASLD, which requires further investigation.

methodsMale C57BL/6 mice were fed a high-fat diet (HFD) for 12 weeks to establish a MASLD mouse model. The lipid level and liver function of mice were evaluated by the levels of TG, TC, ALT, and AST. H&E staining and Oil Red O staining were used to evaluate the pathological changes and lipid deposits in the liver. Lipid metabolism and PPARα/CPT1α signaling pathway-related genes were detected.

resultsLiA effectively reduced weight and improved glucose tolerance and insulin resistance in MASLD mice. LiA treatment significantly reduced lipid accumulation in HFD-induced mice. In addition, bioinformatics analysis, molecular docking, and cellular thermal shift assays further indicated that LiA alleviated MASLD by upregulating PPARα. Furthermore, the protective effect of LiA on lipid accumulation and hepatic steatosis was abolished by PPARα inhibitor (GW7461) pretreatment in MASLD mice.

conclusionThis study demonstrated that LiA ameliorates the lipid metabolism disorder in MASLD mice by upregulating the PPARα/CPT1α signaling pathway.

Indexed as

Carnitine O-PalmitoyltransferaseChalconesFatty LiverLipid MetabolismNon-alcoholic Fatty Liver DiseasePPAR alphaAnimalsDiet, High-FatDisease Models, AnimalLiverMaleMiceMice, Inbred C57BLSignal TransductionUp-RegulationCarnitine O-PalmitoyltransferaseChalconeslicochalcone APPAR alphaPpara protein, mouse

Identifiers

PMID40165660

What Socratic holds

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Registered trials

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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 Socratic graph.