电针通过Bcl-2/Bax/caspase-3信号通路修复海马线粒体损伤改善创伤后应激障碍大鼠的焦虑症状

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Abstract：Objective To investigate the mechanismunderlying the therapeutic efectof electroacupuncture （EA）onposttraumaticstress disorder （PTSD）inrats.MethodsFortymaleSDrats wererandomizedequally intoblankcontrol group，PSD model group，sham-acupuncture group， paroxetine group，and EA group. In the later 3 groups， the rat models of PTSD， inducedbycotiuoussingle-prolongedstresandplantarelecticalstimulatio，wereteatedihEAatV0G18 and BL23 acupoints for 15min （5 times a week for 3 weeks）， sham-acupuncture without electrical stimulation， or gavage with paroxetinesuspensiononthesameschedule.Behavioralchangesof therats wereevaluatedusingopen field test （OFT）and elevated plus maze （EPM）test. Hippocampal pathologies and neuronal changes were examined with HE and Nisl staining， andmitochondrial ultrastructure was examined using electron microscopy.The mRNAand proteinexpression levelsof Bcl-2， Bax，and caspase-3 were detectedbyRT-qPCRand immunofluorescence staining.Results Therat models of PTSDshowed significantlyreducedtotaldistancetraveledinOFnddistanceandtimespentintheopenarmsoftheEPM，witheceased hippocampalneurons，obviousneuronalandmitochondrialpathologies，decreasedhippocampal expressonofB-2and increasedBaxandcaspase-3expressions.TreatmentswithparoxetineandEAbothsignificantlyimprovedbehavioralchanges of theratmodelsincreasedtheumberofNiss-stanedurons，bviouslylleviatedpathologiesinthippocamaluron andmitochondrialultastructure，inreasedhippoapalBcl-2expresionandloweredcaspase-3expresions.Paoetie showedsignificantlybetterefectthanEAforimprovingperformanceoftheatsinEPMtest，whereassham-acupuncturedid notproduceanysignificant improvement.ConclusionEAaleviatesPTSDinratspossblybyupregulating Bcl-2and downregulating Bax and caspase-3， thereby ameliorating hippocampal mitochondrial damage.

Keywords：post-traumaticstrssdisoderlectroacupuncture;iohondria;urons;aspase-3;anietyioder

创伤后应激障碍（PTSD）是个体在经历、目睹或遭遇到严重的恐怖事件、战争、自然灾害等事故后，延迟出现或持续存在的一类精神障碍疾病。（剩余17313字）