1.Inthisstudy,arandomizedandcontrolledmethodwasusedtoobservethetherapeuticeffectsoflive-heart-loadedtherapyonTCMsyndromes,scoresofqualityoflifeandinflammatorycorrelationfactors(IL-18,MMP-9,ppar-γ)inpatientswithcoronaryheartdiseasewithQIdeficiencyandbloodstasis.2.Observingtheeffectoflivingheartonhypoxiacardiomyocytes,andwhetheritcouldinhibittheinflammatoryreactionandenhancetheactivityofhypoxiacardiomyocytesbyculturingcardiomyocytesinvitroandobservethechangesofIL-18,MMP-9,PPAR-γandhif-1αgeneexpressionincardiomyocyteswerestudied.Method1.Thepartofclinic:Inthisstudy,60patientswithcoronaryheartdiseasewithQIdeficiencyandbloodstasisweretreatedbyrandomizedcontrolledmethod,randomlydividedintoliveheartloadinggroup(referredtoasthetreatmentgroup)andconventionaltreatmentgroup(referredtoasthecontrolgroup),eachgroupof30cases,theconventionaltreatmentgrouptogivesimpleWesternmedicinetreatment,liveheartloadinggrouponthebasisofconventionalWesternmedicinetreatmenttoaddthelivingheart(No-fryinggranules),3monthsforonecourseoftreatment,respectively,beforeandaftertreatment,recordingthepatients’serumIL-18,MMP-9,PPAR-γindexes,assessingthesyndromesofTCMsyndromesandevaluatingthequalityoflife,disposalthedatatocollatingandanalyzingit.Finally,analyzinganddiscussingtheresults.2.Thepartofexperiment:Invitrocultureofcardiomyocytes(AC16)andexperimental,throughtheCCK-8anddrugstodeterminethemaximumefficiencyofthetestoftheappropriatelivingheartconcentration.Groupingofculturedcardiomyocytes:includingoxygencontrolGroup(Normoxiagroup),hypoxiawithoutdruggroup(noHXFmeangroup)andhypoxiaplusdruggroup(HXFmeanGroup),respectivelyusingPCR,Westernblotmethodtodetecteachgroupin24,48,72hofIL-18、MMP-9、PPAR-γ、HIF-1αmRNAlevelsandproteinexpression,andanalyzinganddiscussingit.Result1.Theresearchofclinic:(1)TheTCMsymptompointsofthepatientsintheliveheartloadinggroupweresignificantlylowerthanthoseintheconventionaltreatmentgroup,effectiverateis96%(P<0.05);(2)Thequalityoflifescaleofpatientswithliveheartloadinggroupwassignificantlyhigherthanthatofconventionaltreatmentgroup.（）3)TherewasnosignificantdifferenceinserumIL-18levelcomparedwithconventionaltreatmentgroupinpatientswithliveheartloadinggroup.(P>0.05);TheserumMMP-9levelofthepatientsintheliveHeartloadinggroupwassignificantlylowerthanthatintheconventionaltreatmentgroup,itisstatisticallysignificantbycomparingit’sdifference(P<0.05);TheserumPPAR-γlevelofthepatientswithliveheartloadinggroupwassignificantlyhigherthanthatintheconventionaltreatmentgroup,anditisstatisticallysignificantbycomparingit’sdifference.（）2、TheexperimentalStudyinvitro:(1)CCK-8anddrugmaximumefficiencypre-test:Choosetherightlivingheartoftheconcentrationof1%,thelivingheartofnormalmyocardialcellswithoutsignificanteffect();(2)Afterhypoxiatreatment6h,theexpressionlevelofIL-18,MMP-9andhif-1αofcardiacmyocytesincreased,PPAR-γexpressionleveldecline;(3)Undertheconditionofhypoxia,theexpressionlevelofIL-18andMMP-9ofcardiomyocytesinhypoxiaplusdruggroupwassignificantlylowerthanthatofhypoxiawithoutdruggroup(P<0.05andtheexpressionlevelofPPAR-γandhif-1αinhypoxiaplusdruggroupwashigherthanthatofhypoxiawithoutdruggroup(P<0.05)结论1.ThetreatmentofcoronaryheartdiseasewithliveheartcanreducetheMMP-9levelofinflammatoryfactor,promotingtheexpressionofPPAR-γlevel,improvingtheclinicalsymptomofpatientsandenhancingthequalityoflife.2.Undertheconditionofoxygen-poor,theexpressionlevelofhif-1α,MMP-9andIL-18ofcardiomyocyteswillincreased,theexpressionlevelofPPAR-γdecreased,theexpressionofIL-18andMMP-9couldbereducedeffectively,andtheactivityofhif-1αandPPAR-γcouldbeimprovedandtheinflammationreactioncouldbesuppressed.Enhancehypoxiaadaptabilitytoplayaroleinprotectingcardiomyocytes.KEYWOEDS:Livingheart,coronaryheartdisease,deficiencyofbloodstasistype,clinicaleffects,anoxicmyocardialcells,inflammatoryfactors
