低氧對(duì)團(tuán)頭魴細(xì)胞凋亡與抗氧化酶活性的影響

低氧對(duì)團(tuán)頭魴細(xì)胞凋亡與抗氧化酶活性的影響

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時(shí)間:2019-02-28

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1、萬方數(shù)據(jù)華中農(nóng)業(yè)大學(xué)2015屆碩士研究生學(xué)位論文mg/L)中,兩者的值又有所回升。4.低氧對(duì)肝臟抗氧指標(biāo)的影響對(duì)不同低氧組團(tuán)頭魴肝臟各種抗氧化酶指標(biāo)的檢測(cè)結(jié)果顯示,低氧會(huì)導(dǎo)致肝臟中SOD和CAT酶活性、過氧化氫(H202)降低。肝臟中一氧化氮(NO)水平隨溶氧濃度的降低及低氧處理時(shí)間的延長逐漸增加。肝臟總ROS水平隨著低氧處理時(shí)間的延長逐漸降低,而復(fù)氧及嚴(yán)重低氧時(shí)ROS含量回升。關(guān)鍵詞:團(tuán)頭魴;低氧;細(xì)胞凋亡;心臟;TUNEL萬方數(shù)據(jù)低氧對(duì)團(tuán)頭魴細(xì)胞凋亡及抗氧化酶活性的影響AbstractMegalobramaamb

2、lycephala,alsocalledWuchangfish,isakindofimprovedeconomicfreshwaterfish.Inrecentyears,withthedeteriorationofnaturalenvironmentandhumanactivityintervention,itslivingenvironmentoftenappearedlowoxygen,restrictingthedevelopmentof彪amblycephalabreeding.Inourstudy,the

3、structurechangesofdifferenttissuesofMamblycephalawereobservedafterhypoxiatreatment,andtheactivitiesofantioxidantenzymeswereanalyzedintheliverinhypoxiaandhypoxia-recoveryconditions.Theinfluenceoflowoxygenonmyocardialcellapoptosisandbcl-2expressionwerealsostudied

4、byTUNELandfluorescencequantitativePCR.Additionally,thechangesofMDAcontentandSODactivitywereanalyzedinheartmitochondriaextractedusingsucrosegradientcentrifugationmethod.Themainresultswereasfollows:1.Effectsofhypoxiaonstnl曲lreofdifferenttissuesofM.a(chǎn)mblycephalaDif

5、ferenttissues(heart,liver,kidney,muscle,spleen)weresampledandobservedbasedonHEstainingafterseverehypoxictreatment(DO:0.5mg/L),andtheresultsrevealedthatgreaterinfluenceofhypoxiaontheheartandkidney,whichmusclefmersinheartshowedswellinganddisorderinarrangementinse

6、verehypoxiaconditions,brokencapillarieswereobservedinspleen.However,hypoxiae虢ctsonstructureofmuscle,liverspleenwererelativelylesser.Theresultsshowedbasedonelectronmicroscopethatundermoderatehypoxia(DO:2.5+0.5mgmfor2h,4”,myocardialmitochondrialstructurewerebroke

7、n,mitochondriaWasswellinganddisorder,butinserverhypoxia(DO:O.5mg/L),somemitochondriawerefractured.2.CardiaccellapoptosiscausedbyhypoxiaInordertofurtherstudyhypoxiae毹ctsonhearttissueofMamblycephala,cardiaccellapoptosisandbcl-2mRNAlevelswereanalyzedbyTUNEL(termin

8、aldexynucleotidyltransferaseTdTmediateddUTPNickendlabeling)andfluorescencequantitativePCRafterhypoxiatreatment.Theresultsshowedthathypoxiainducedcardiaccellapoptosis,andwith

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