‘气经-血络"截断动脉粥样硬化斑块形成：降脂化斑方调控小鼠肝脏逆向胆固醇转运途径改善动脉粥样硬化的机制

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Abstract：Objective ToexplorethemolecularmechanismofJiangzhi Huaban Decoction （JZHBD）forimprovingatherosclerosis throughthe"qimeridian-bloodchannels"pathway.MethodsApoEmousemodelsofatherosclerosiswereestablishedbyhigh fatdietfeedingfor8weeks，withC57BL/6miceonanormaldietasthecontrols.FortyApoEmousemodelswererandomized intomodelgroup，low-，medium-andhighdoseJZHtreatmentgroups，andatorvastatintreatment group（n=8）fortheir respectivetreatmentsfor8weeks.Thechangesinbodyweightandoverallconditionofthemiceweremonitoredwekly.After thetreatsdd intheliverandaorticrotplaques wereexaminedwithHEstaining，andlipidacumulationintheliverandaorticwall was assessedusingOilRedOstaining.Thecoremolecularmechanismwasstudiedthroughtranscriptomics，andtheexpresionsof thekeypathwayproteins wereconfirmedusing Westemblotingandimmunohistochemistry.Results Treatmentwith JZHBD significantlyeducedbloodlipidandtotalbilecidlevels，improedliverfunctioandpaticsteatosis，andeceaotic lipiddepositionandplaqueareainthemousemodelsofatherosclerosis.Transcriptomicanalysissuggestedthatthe therapeuticmechanismofJZHBDinvolvedreversecholesterol transport，PPARsignalingandtheinflammatorypathways.In atheroscleroticce，JZHtreatmentobviouslyup-regulatedpaticexpresinsofPARy，XRa，ABCA1，ABCG1and CYP7A1，doratedticepsof/561βinteeeed5de intheintestinesanddecreasedICAM-1and VCAM-1expresionsintheaorticplaques.ConclusionJZHBDimproves atheroscleroticvasculardamageandplaque formationpossiblybyregulating hepaticreversecholesteroltransportand inflammation via modulating the hepatic PPARy/LXRa/NF-kB signaling pathway.

Keywords：atherolerosis;qimeridian-bloodanels;JangzhiHuabanDecoctio;everseolesteroltrasprt;vasulacel adhesionmolecules

动脉粥样硬化（AS）是由于脂质在中、大动脉内壁的逐渐累积，引起血流减少或血管堵塞，其病理状态进展缓慢且持续。（剩余15506字）