简介：ThepresentstudywasdesignedtodeterminetheeffectsofatraditionalChinesemedicine,calledQishenYiqiDroppingPillonchronichypoxia-inducedmyocardialinjury.ToestablisharatchronichypoxiamodeltobeusedintheevaluationofthetherapeuticeffectsoftheQishenYiqiDroppingPill,Sprague-Dawley(SD)ratswererandomlydividedintothreegroups:thecontrol,model,andtreatmentgroups(n=10pergroup).Theanimalswerehousedinaplexiglasscontainer.Thecontrolanimalswereundernormaloxygenconcentrationandthemodelandtreatmentgroupswereexposedtoairandnitrogenfor5weeks.TheratsinthetreatmentgroupwereorallyadministeredtheQishenYiqiDroppingpill(35mg·kg-1·d-1)for5weeks.Afterthetreatment,thecardiacfunctionandmorphologywereanalyzed,andtheexpressionlevelsofhypoxia-induciblefactor1α(HIF-1α)weredeterminedusingWesternblotting.Ourresultsindicatedthatthecardiacfunctionwasimpaired,cellapoptosiswasenhanced,andHIF-1αexpressionwasup-regulatedinthemodelgroup,comparedtothecontrolgroup.ThesechangeswereamelioratedbythetreatmentwiththeQishenYiqiDroppingPill.Inconclusion,QishenYiqiDroppingpillcanamelioratemyocardialinjuryinducedbychronichypoxia,improvecardiacfunction,anddecreasemyocardialcellapoptosis,whichmayprovideabasisforitsclinicaluseforthetreatmentofchroniccardiovasculardiseases

简介：Sheng-Mai-San(SMS),awell-knownChinesemedicinalplantformula,iswidelyusedforthetreatmentofcardiacdiseasescharacterizedbydeficiencyofQiandYinsyndrome.Amousechronicintermittenthypoxia(CIH)modelwasestablishedtomimictheprimaryclinicalfeaturesofdeficiencyofQiandYinsyndrome.MiceexperiencedCIHfor28days(nadir7%topeak8%oxygen,20minperday),resultinginleftventricle(LV)dysfunctionandstructureabnormalities.AfteradministrationofSMS(0.55,1.1,and5.5g·kg-1·d-1)forfourweeks,improvedcardiacfunctionwasobserved,asindicatedbytheincreaseintheejectionfractionfromtheLVonechocardiography.SMSalsopreservedthestructuralintegrityoftheLVagainsteccentrichypotrophy,tissuevacuolization,andmitochondrialinjuryasmeasuredbyhistology,electronmicroscopy,andultrasoundassessments.Mechanistically,theantioxidanteffectsofSMSweredemonstrated;SMSwasabletosuppressmitochondrialapoptosisasindicatedbythereductionofseveralpro-apoptoticfactors(Bax,cytochromec,andcleavedcaspase-3)andup-regulationoftheanti-apoptosisfactorBcl-2.Inconclusion,theseresultsdemonstratethatSMStreatmentcanprotectthestructureandfunctionoftheLVandthattheprotectiveeffectsofthisformulaareassociatedwiththeregulationofthemitochondrialapoptosispathway.