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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–rayestablishmentofcardiacmyocytedamagemodelan
2、dtheinterventionbydifferentconcentrationofAPS.Theexperimentwasdividedintothefollowingfivegroups:Normalcontrolgroup;Radiationdamagemodelgroup(6Gy);Low-doseAPSintervenetiongroup(0.025mg/mL);Medium-doseAPSinterventiongroup(0.05mg/mL);High–doseAPSinterven
3、etiongroup(0.1mg/mL).ThegrowthinhibitionrateofmyocardialcellsofeverygroupswasassessedusingMTTassay;Thecellcycleandapoptosisofeverygroupswasdetectedbyflowcytometry;Themitochondrialfunctionofeverygroupswasevaluatedbylaserconfocalmicroscope;ThelevelsofRO
4、SofeverygroupswasmeasuredbyfluorescentprobeDCFH-DA;TheproteinexpressionofCytC,caspases-3,caspases-9inthemyocardialcellsofeverygroupsweredeterminedwithwesternblotmethod.Result:Thecardiacmyocyteofnormallyculturedwereroundshape,butafterradiationdamage,th
5、eyareturnedroundandfloatedatdifferentlevelsthecellapoptosishadbegan.Comparedwiththenormalgroup,themodelgroupshowedthatthegrowthinhibitionrateofcardiacmyocytewasincreased,theX-raycanprolongtheperiodandincreasestheapoptosisratioofcardiacmyocyte,themitoc
6、hondrialdisorderinmodelgroupandtheΔΨmdecreased,thelevelsofROS,CytC,caspases-3,caspases-9expressionincreased（p＜0.05）.Comparedwiththemodelgroup,theAPSinterventiongroupsshowedthatthegrowthinhibitionrateofcardiacmyocytewasdecreased,thecellcycleshortenedan
7、dtheapoptosisratioofcardiacmyocytedecreased,themitochondrialfunctionimprovedandtheΔΨmincreased,thelevelsofROSCytC,caspases-3,caspases-9expressiondecreased（p＜0.05）.Conclusions:1.APScanprotectagainstmitochondriafunctionofcardiacmyocyteinjuredbyRadiation
8、inneonatalratsthroughchuckingawayROS,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
