清心牛黄丸通过改善脂质代谢紊乱缓解小鼠非酒精性脂肪性肝病

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Abstract：ObjectiveToinvestigatetheefectofChingShumPills（CSP）foralleviatingnon-alcoholicfattyliverdisease （NAFLDandtheunderlyingmechanism.MethodsInamousemodelofNAFLD，thetherapeuticefectofCSPwasevaluated by measuringserumgucose，lipidprofiles （TC，G，D-C，HD-C），andepaticfunctionmarkers.Networkpcolgy wasemployedtifctieoosideirgetsinPRBgeteictios OMIM，and DisGeNET.Protein-protein interaction （PPI） networks，GeneOntology （GO），and KEGG pathway analyses were conducted.Molecular docking （AutoDock Vina）wasused toassssthecompound-target bindingafinities.Quantitativerealtime PCR （qRT-CR） wasused to validate the mRNA expresions of the core genes inthe liver tisseof the mouse models. Results In the mouse model of NAFLD，treatment with CSP significantly reduced body weight gain and serum TG levels of themice，andhigh-doseCSPtreatmentresulted inobviousreductionofALTlevelsandhepaticfataccumulation.Network pharmacologyaalysisidentifiedquercetinad-monolinoleninasthekeybioactivesinCSP，whichargetTF，6， TP53，and ALB.Dockingsimulationssuggested strong bindingbetweenthetwocorecompoundsandtheirtargetproteins.The resultsofqR-PCRshowedthathigh-fatdietinducedsignificantdownegulationofTp53，CptandPparaexprionsin mice，which was efectivelyreversedbyCSPtreatment.ConclusionCSPcanimprove lipid metabolismdisordersinNAFLD micethrougharegulatorymechanisminvolvingmultipletargetsandpathwaystoreduceliverfataccumulationandprotect liver function.The keycomponents in CSPsuchasquercetinandlinolenicacid monoacylglycerol mayparticipate inthe regulation of such metabolic processes as fatty acid oxidation by targeting TP53.

Keywords： non-alcoholicfatty liverdisease;Ching ShumPills;quercetin; lipidmetabolism;liver function

非酒精性脂肪性肝病（NAFLD）是指在无饮酒和其他因素的情况下，出现以肝脏脂肪变性和堆积为特征的代谢性肝损伤[1-4]。（剩余14019字）