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1、黄芪多糖对辐射致乳鼠心肌细胞损伤的保护作用及其机制探讨AbstractObjective:ToinvestigatetheeffectofAPSonantiradiationdamageincardiacmyocytesanditsmechanism.Methods:Primaryextractiontechniquessuccessfullyculturedmyocardialcellsinvitro,X–rayestablishmentofcardiacmyocytedamagemodelandt
2、heinterventionbydifferentconcentrationofAPS.Theexperimentwasdividedintothefollowingfivegroups:Normalcontrolgroup;Radiationdamagemodelgroup(6Gy);Low-doseAPSintervenetiongroup(0.025mg/mL);Medium-doseAPSinterventiongroup(0.05mg/mL);High–doseAPSintervenetio
3、ngroup(0.1mg/mL).ThegrowthinhibitionrateofmyocardialcellsofeverygroupswasassessedusingMTTassay;Thecellcycleandapoptosisofeverygroupswasdetectedbyflowcytometry;Themitochondrialfunctionofeverygroupswasevaluatedbylaserconfocalmicroscope;ThelevelsofROSofeve
4、rygroupswasmeasuredbyfluorescentprobeDCFH-DA;TheproteinexpressionofCytC,caspases-3,caspases-9inthemyocardialcellsofeverygroupsweredeterminedwithwesternblotmethod.Result:Thecardiacmyocyteofnormallyculturedwereroundshape,butafterradiationdamage,theyaretur
5、nedroundandfloatedatdifferentlevelsthecellapoptosishadbegan.Comparedwiththenormalgroup,themodelgroupshowedthatthegrowthinhibitionrateofcardiacmyocytewasincreased,theX-raycanprolongtheperiodandincreasestheapoptosisratioofcardiacmyocyte,themitochondrialdi
6、sorderinmodelgroupandtheΔΨmdecreased,thelevelsofROS,CytC,caspases-3,caspases-9expressionincreased（p＜0.05）.Comparedwiththemodelgroup,theAPSinterventiongroupsshowedthatthegrowthinhibitionrateofcardiacmyocytewasdecreased,thecellcycleshortenedandtheapoptosi
7、sratioofcardiacmyocytedecreased,themitochondrialfunctionimprovedandtheΔΨmincreased,thelevelsofROSCytC,caspases-3,caspases-9expressiondecreased（p＜0.05）.Conclusions:1.APScanprotectagainstmitochondriafunctionofcardiacmyocyteinjuredbyRadiationinneonatalrats
8、throughchuckingawayROS,shorteningcellcycle,stabilizingtheΔΨm,decreasingtheexpressionofCytC,caspases-3,caspases-9.2.APScanprotectagainstmitochondriafunctionofcardiacmyocyteinjuredby2万方数据黄芪多糖对辐射致乳鼠心肌细胞损伤的保护作用及其机制探讨Radiationinneonat
