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1、黃芪多糖對輻射致乳鼠心肌細(xì)胞損傷的保護(hù)作用及其機(jī)制探討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.APScanprotectagainstmitochondriafunctionofcardiacmyocyteinjuredby2萬方數(shù)據(jù)黃芪多糖對輻射致乳鼠心肌細(xì)胞損傷的保護(hù)作用及其機(jī)制探討Radiationinneonat