依达拉奉对局灶性脑缺血大鼠脑组织水通道蛋白9mrna表达的影响

《依达拉奉对局灶性脑缺血大鼠脑组织水通道蛋白9mrna表达的影响》由会员上传分享，免费在线阅读，更多相关内容在行业资料-天天文库。

1、Abstractpoint(p<0.05).Thechangetendencywasnearlythesameasthatofthebrainwatercontent.ThecorrelationanalysisdemonstratedthatexpressionlevelofAQP9mRNAwascorrelatedapparentlywiththebrainwatercontent(r=0.788,p<0.05).⑸Theinfarctvolumeintheedaravonetreatgroupandthephysiologic

2、alsalinegroupreacheditspeakat24hourspostischemia.Comparedwiththephysiologicalsalinegroup,theinfarctvolumeintheedaravonetreatgroupwasdecreasedmanifestlyduring6～24haftercerebralischemiainphysiologicalsalinegroup(p<0.05).⑹TheHEstainofthephysiologicalsalinegroupindicatedth

3、attheshapeofneuronsaroundtheischemicregionhadnoobviouschangesat6h.At6hpostischemia,braintissuesaroundtheischemicfocuswereobviouslyswollenandnecrotic.Thepathematologydamagesuchasbrainedemaandneuronnecrosiswasamelioratedsignificantlyintheedaravonetreatgroup.Intheshame-op

4、eratedgroup,therewerenosignificantchangesinthebraintissue.Conclusion:⑴Theexperimentdemonstratesthattheratmodeloffocalcerebralischemiamadesuccessfullybyusingtheintraluminalsutureinthisstudywasreliableandreproducible.Themodelissimilartoclinicalcerebralischemia.Itisapplic

5、abletotheacuteempiricalstudy.⑵TheAQP9mRNAexpressionlevelinthephysiologicalsalinegroupisalsosignificantlyhigherthantheshame-operatedgroup.Moreover,theup-regulatedexpressionofAQP9mRNAandthebrainwatercontentarealsoconsistentaftercerebralischemicateachtimepoint.Thisimplies

6、thatUp-regulatedAQP9mRNAexpressioniscloselyassociatedwiththeoccurrenceanddevelopmentofbrainedemaaftercerebralischemic.AndAQP9mightplayanimportantroleinbrainedemaformationandthesecondaryneuronalinjuryaftercerebralischemic.⑶Edaravone,asafreeradicalscavengingagent,caninhi

7、biteffectivelytheexpressionofAQP9mRNAandattenuatebrainedema.ItisassumedthattheinhibitionofAQP9mRNAexpressiontorelievecerebraledemamaybethemechanismsofedaravoneneuroprotection.ModificationofAQP9mRNAactivityandregulationofAQP9mRNAexpressionlevelwouldbethenewstrategytopre

8、ventthecerebraledemaandtoreducecerebralinjuryafterstroke.Whichimplythatthetherapeuticstrategytargetedtomodulationwith