參麥注射液對外傷性腦損傷大鼠神經(jīng)元細胞的保護作用

1、28主墾主亙醫(yī)堡金魚墊盤查；!生!旦箜!鲞箜!塑璺壘墮!堡叢里堅墾塵曼!堡!翌!翌!：!墮!：!論著參麥注射液對外傷性腦損傷大鼠神經(jīng)元細胞的保護作用白玉，張圣土拳，王良榮，趙喜悅，林麗娜(溫州醫(yī)學(xué)院第一附屬醫(yī)院麻醉科，浙江溫州325000)【摘要】目的探討參麥注射液對外傷性腦損傷的保護機制。方法按隨機數(shù)字表法將72只雄性SD大鼠分為假手術(shù)組、模型組、參麥治療組，每組24只。采用改良Freeney法制作外傷性腦損傷大鼠模型；假手術(shù)組單純開骨窗不損傷腦組織。參麥治療組于傷后1h單次腹腔注射參麥注射液15mlkg；模型組給予等量生理鹽水。傷后6、10、24及72h檢測血清神經(jīng)元特異性烯醇化酶(NSE

2、)、超氧化物歧化酶(SOD)及丙二醛(MDA)水平，同時觀察腦組織病理改變，于24h觀察大鼠平衡木實驗(BBT)評分。結(jié)果光鏡下觀察假手術(shù)組各時間點腦組織結(jié)構(gòu)正常，無出血、水腫及損傷；與模型組相比，參麥治療組大鼠損傷灶周圍腦細胞缺氧、水腫損傷程度及損傷范圍均有明顯改善。與假手術(shù)組比較，模型組和參麥治療組早期NSE含量顯著升高，均于傷后6h達峰值(5133士570)pgL、(4341士521)ggL比(1433士326)pgL，均尸<0013，72h基本恢復(fù)；SOD活性顯著下降，均于傷后24h達谷值(17934士514)kUL、(19260士657)kUL比(20523士808)kUL，P

3、<001和P<o053。與模型組比較，參麥治療組各時間點NSE含量下降，SOD活性升高(P<005或P<001)。各組各時間點間MDA含量均無明顯變化。參麥治療組BBT評分較模型組增高(2250士0420)分比(1875土0440)分，但差異無統(tǒng)計學(xué)意義(P>o05)。結(jié)論增強SOD活性、減少NSE產(chǎn)生、保護神經(jīng)元細胞可能是參麥注射液保護外傷性腦損傷的作用機制。【關(guān)鍵詞】腦損傷，外傷性；神經(jīng)元特異性烯醇化酶；超氧化物歧化酶；參麥注射液中圖分類號：R2855；R65115ProtectionofShenmai文獻標(biāo)識碼：AneuronDOI：103969jissn1

4、0089691201001009cellsinratsinjection(參麥注射液)onaticbrainfollowingtrauminjuryBAItheFirstYu，ZHANGSheng-gong，WepartmentofANGLiangrang，ZHAOXi-yue，L，Li一觸DWenzhouMedicalAffiliatedHCollege，Wenzhou325000,Zhefiang，ChinaospitalofAnesthesiology，Correspondingauthor：LLirid，Email：wzlirdinatomcoTnAbstractObjectivetr

5、aumaticbrainaiToinvestigatetheprotectionofShenminjection(參麥注射液)inratsfollowingeredividedintothreeinjury(TBI)MethodsSeventytwoSpragueDawley(SD)maleratswethod(eachn=24)：theshamoperation，themodelandtheShenmaiinjection-groupsbyrandomdigitstablemtreatedgroupsThelattertwogroupsreceivedfreefallinjuryinthec

6、erebralhemethod)isphere(FreeneymTheShenmaiinjectiontreatedgroupreceivedrouteonceaiofintraperitonealShenmatinjection(15mlkg)，andthemodelgroup。thesameaspostinjuryApieceofskullwtakenawithoutcerebralinjuryTayintheshamoperationgroupwhelevelsofserumneuronspecificenolaseutase(soD)andmeasuredat6，10，24，72hou

7、rs(NSE)，superoxidedismalondialdehyde(MDA)weremafterTBI。andinthemeantime，thepathologicalchangesofratsanddoseofisotonicsodiumchloride1hourbraintissueswereobservedTheabilityofatusclemovementcoordinatingmmicroscope，thevariousofandkeepingbalanceinwasassessedno24hoursResultsUnderlightthearstructurehemorrh

8、age，edemaandinjuryattimepointsintheshamoperationgroup；incomwiththemodelparisongroup，thehypoxia，edemaandeaofinjuryofthebraincellsaroundthefoCUSofinjuryweresignificantlyimaiprovedintheShenmbraintissuewasnormalandtherewereSEinthemodelandtheinjectiontreatedgroupComparedwiththeshamoperationgroup，thelevel

9、sofNereincreasedsignificantlywithapeakat6hoursCShenmaiinjectiontreatedgroupsw(5133土570)pgL，returned(4341士521)肛gLvs(1433士326)腿L，bothP<001andtheybasicallytothebaselinelevelat72hoursafterTBITheactivitiesofSODwereremarkablyreducedwithavalleyat24hoursL，P<O01andP<005)C(17934士514)kUL，(19260士657)kU

10、Lvs(20523士808)kUSEwaslower，theactivityofSODwashigherintheShenmaiiththemodelgroup，thelevelofNComparedwepoints(P<O05orP<O01)Throughoutthisstudy。nostatisticalinjectiontreatedgroupatvarioustiminthethreewereobservedThescoreofbalancingbeamtest(BDAgroupsBT)wassignificantchangesofMaihigherintheShenmbu

11、ttherewasnoodelgroup(1875士0440)，injectiontreatedgroup(Z250士0420)thanthatinthemstatisticalsignificantedifference(P>005)ConclusionEnhancingtheactivityofSODandcellsinSEarinhibitingtheproductionofNratsechanismsofpossiblythemShenmaiinjectioninprotectingneuronfollowingTBIordsTraumaticKeywbraininjury；Neuronutase，Shenmaispecificenolase；Superoxidedisminjection參麥注射液是由人參、麥冬組成的中藥注射劑，基金項目：浙