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

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dc.contributor.authorHongfeng Xu
dc.contributor.authorRui Yan
dc.contributor.authorLuqi Qiu
dc.contributor.authorGuojun Wang
dc.contributor.authorYantao Zhu
dc.contributor.authorWenrui Zhu
dc.contributor.departmentBiología Celular e Histología
dc.date.accessioned2025-11-11T08:52:58Z
dc.date.available2025-11-11T08:52:58Z
dc.date.issued2025
dc.description.abstractBackground. Metabolic 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. Methods. Male 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. Results. LiA 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. Conclusion. This study demonstrated that LiA ameliorates the lipid metabolism disorder in MASLD mice by upregulating the PPARα/CPT1α signaling pathway.
dc.formatapplication/pdf
dc.format.extent13
dc.identifier.doihttps://doi.org/10.14670/HH-18-907
dc.identifier.eissn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/172109
dc.languageeng
dc.relationSin financiacion externa a la Universidad
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectLicochalcone A
dc.subjectPPARα
dc.subjectLipid metabolism
dc.subjectMetabolic dysfunction associated steatotic liver disease
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleLicochalcone A ameliorates lipid accumulation in metabolic dysfunction-associated steatotic liver disease via upregulating PPARα/CPT1α
dc.typeinfo:eu-repo/semantics/article
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Histology and histopathology, Vol.40, Nº12, (2025)