Reperfusion Promotes Mitochondrial Dysfunction following Focal Cerebral Ischemia in Rats 英文参考文献.docVIP

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Reperfusion Promotes Mitochondrial Dysfunction following Focal Cerebral Ischemia in Rats 英文参考文献.doc

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Reperfusion Promotes Mitochondrial Dysfunction following Focal Cerebral Ischemia in Rats 英文参考文献

ReperfusionPromotesMitochondrialDysfunction followingFocalCerebralIschemiainRats JunLi1,XuesongMa1,WeiYu1,ZhangqunLou1,DunlanMu1,YingWang1,BaozhongShen2*,SihuaQi1* 1DepartmentofAnesthesiology,theFourthAffiliatedHospital,HarbinMedicalUniversity,Harbin,China,2MolecularImagingKeyLaboratoryofGeneralUniversitiesand CollegesofHeilongjiangProvince,Harbin,China Abstract Background and Purpose: Mitochondrial dysfunction has been implicated in the cell death observed after cerebral ischemia,andseveralmechanismsforthisdysfunctionhavebeenproposed.Reperfusionaftertransientcerebralischemia maycausecontinuedandevenmoreseveredamagetothebrain.Manylinesofevidencehaveshownthatmitochondria sufferseveredamageinresponsetoischemicinjury.Thepurposeofthisstudywastoobservethefeaturesofmitochondrial dysfunctioninisolatedmitochondriaduringthereperfusionperiodfollowingfocalcerebralischemia. Methods: Male Wistar rats were subjected to focal cerebral ischemia. Mitochondria were isolated using Percoll density gradient centrifugation. The isolated mitochondria were fixed for electron microscopic examination; calcium-induced mitochondrial swelling was quantified using spectrophotometry. Cyclophilin D was detected by Western blotting. Fluorescent probes were used to selectively stain mitochondria to measure their membrane potential and to measure reactiveoxidativespeciesproductionusingflowcytometricanalysis. Results:Signsofdamagewereobservedinthemitochondrialmorphologyafterexposuretoreperfusion.Themitochondrial swellinginducedbyCa increasedgraduallywiththeincreasingcalciumconcentration,andthistendencywasexacerbated 2+ as the reperfusion time was extended. Cyclophilin D protein expression peaked after 24hours of reperfusion. The mitochondrialmembranepotentialwasdecreasedsignificantlyduringthereperfusionperiod,withthegreatestdecrease observed after 24hours of reperfusion. The surge in mitochondrial reactive oxidative species occurred after 2hours of reperfusionandwasmaintainedatahighlevelduringther