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二氢杨梅素通过调控NLRP3炎症小体减轻LPS诱导鸡肝损伤的作用机制研究.docx

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二氢杨梅素通过调控NLRP3炎症小体减轻LPS诱导鸡肝损伤的作用机制研究 Title:MechanisticInsightsintotheProtectiveEffectsofDihydromyricetinonLPS-InducedChickenLiverInjurythroughNLRP3InflammasomeModulation Abstract: Dihydromyricetin(DHM),aflavonoidcompoundderivedfromtheAmpelopsisgrossedentataplant,hasbeenreportedtoexhibitpotentanti-inflammatoryproperties.Inthisstudy,weaimedtoinvestigatetheunderlyingmechanismsbywhichDHMattenuateslipopolysaccharide(LPS)-inducedliverinjuryinchickensthroughmodulationoftheNLRP3inflammasome. Introduction: Liverinjuryisacommonpathologicalconditionassociatedwithvariousfactors,includingexposuretobacterialendotoxinLPS.TheNLRP3inflammasomeisacriticalcomponentoftheinnateimmunesystemandhasbeenimplicatedinthedevelopmentandprogressionofliverinjury.Dihydromyricetinhasbeenshowntopossessanti-inflammatoryproperties;however,theprecisemechanismsbywhichDHMprotectsagainstLPS-inducedliverinjuryremainlargelyunknown. Methods: Inthisstudy,aninvivochickenmodelofLPS-inducedliverinjurywasestablished.DHMwasadministeredorallytotheexperimentalgroup,whilethecontrolgroupreceivedavehicle.Liverfunctiontestsandhistopathologicalexaminationswereperformedtoassesstheextentofliverinjury.Inflammatorycytokinesandoxidativestressmarkerswerequantifiedtoevaluatetheanti-inflammatoryeffectsofDHM.Furthermore,theexpressionlevelsofNLRP3inflammasome-relatedproteinsweremeasuredtoelucidatethemodulatoryeffectsofDHMontheNLRP3inflammasomepathway. Results: AdministrationofDHMsignificantlyamelioratedLPS-inducedliverinjury,asevidencedbyreducedserumlevelsofALTandAST,decreasedhepaticinflammation,andattenuatedhistopathologicalchanges.Moreover,DHMtreatmentsuppressedthereleaseofpro-inflammatorycytokines,suchasinterleukin-1β(IL-1β)andinterleukin-18(IL-18),whileincreasingthelevelsofanti-inflammatorycytokineinterleukin-10(IL-10).Additionally,DHMmitigatedoxidativestressbydecreasingmalondialdehyde(MDA)levelsandenhancingsuperoxidedismutase(SOD)activity. Furthermore,DHMtreatmenteffectivelydownregulatedtheproteinexpressionofNLRP3,ASC,andcaspa