摘要
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.
出版日期
2015年10月20日（中国期刊网平台首次上网日期，不代表论文的发表时间）
