神经生长抑制因子Nogo―A在大鼠脑梗死后功能恢复中的作用机制[摘要]目的探?大鼠脑梗死后功能恢复过程中神经生长抑制因子Nogo-A的表达水平。方法选取雄性SD大鼠60只，采用随机数字表法分为对照组和模型组，每组各30只。模型组制备MCAO模型，对照组行假手术处理，各组于术后第3、7、28天三个时间点随机取10只进行检测，原位杂交法和Westernblot法检测Nogo-AmRNA和蛋白表达，采用Longa评分标准对神经功能评分，HE染色观察分析神经元形态。结果模型组术后Nogo-AmRNA和蛋白表达明显高于对照组（P<0.05）；模型组术后第7天Nogo-AmRNA和蛋白表达量明显高于术后第3、28天（P<0.05），而术后第28天明显低于术后第3天（P<0.05）；HE染色显示，对照组神经元形态正常，模型组神经元形态异常，其中模型组第7天细胞形态、梗死状况及周围炎性反应较第3、28天重；模型组术后神经功能评分明显高于对照组（P<0.05）；模型组术后第28天神经功能评分明显低于术后第3、7天（P<0.05）。结论大鼠脑梗死后Nogo-A表达明显升高，可能与损伤后神经再生障碍有关。[关键词]脑梗死；Nogo-A；MCAO模型；大鼠[]R743.3[文献标识码]A[]1673-7210（2017）03（b）-0016-04ActionmechanismofneuronalinhibitoryfactorNogo-AonratsinfunctionalrecoveryaftercerebralinfarctionMayila?Tuerxun1A激aer?Muheda1Sanubaer?Maimaiti2Tuerxun?Shabier11.DepartmentofNeurology，theFirstAffiliatedHospitalofXin激angMedicalUniversity，Xin激angUygurAutonomousRegion，Urumqi830054，China；2.DepartmentofNeurology，theFifthAffiliatedHospitalofXin激angMedicalUniversity，Xin激angUygurAutonomousRegion，Urumqi830011，China[Abstract]ObjectiveTodiscussNogo-Aexpressionofnervegrowthinhibitorincerebralinfarctionratsduringfunctionalrecovery.Methods60maleSDratswererandomlydividedintotwogroups：controlgroupandmodelgroupbyrandomnumbertablemethod，30ratsineachgroup.ThemodelgroupwerepreparedwithMCAOmodel，andthecontrolgroupweretreatedwithshamoperation.10ratswererandomlychosentotestedfromeachgroupinpostoperative3，7，28d.NeuronalmorphologywasobservedbyusingHEstaining，andtheNogo-AmRNAandproteinexpressionweretestedinsituhybridizationandWesternblotmethod，Longascorestandardwereusedtoscorednervefunction.ResultsNogo-AmRNAandproteinexpressioninmodelgroupwassignificantlyhigherthanthatincontrolgroup（P<0.05）.Nogo-AmRNAandproteinexpressioninpostoperative7dofmodelgroupweresignificantlyhigherthanthatinpostoperative3，28d（P<0.05）.Nogo-AmRNAandproteinexpressioninpostoperative28dweresignificantlylowerthanthatinpostoperative3d（P<0.05）.HEstainingshowednormalmorphologyofneuronsincontrolgroupandabnormalmorphologyofneuronsinmodelgroup，andthecellmorphology，myocardialinfarctionandperipheralinflammatoryresponseinmodelgroupof7daysweremoreseriousthan3，28d.Theneurologicalfunctionscoresinmodelgroupwassignificantlyhigherthanthatincontrolgroup（P<0.05）.Theneurologicalfunctionscoreinpostoperative28dwassignificantlylowerthanthatinpostoperative3，7d（P<0.05）.ConclusionNogo-Aexpressionsignificantlyincreaseincerebralinfarctioninrats，whichmayberelatedtothenerveregenerationdisordersafterinjury.[Keywords]Cerebralinfarction；Nogo-A；MCAOmodel；Rat脑梗死是一种由多因素作用引起的脑部缺血、缺氧进而诱发的局限性脑组织缺血性坏死或软化疾病。本病存在明显高危特征，具有极高致死和致残率，严重威胁人类安全[1-3]。脑梗死发病后患者神经系统存在明显损伤，并且介入治疗后恢复难度也较大，其原因可能为：①患者中枢神经系统内在特性损伤，缺乏再生能力；②中枢神经系统内某些物质抑制而出现再生功能损伤[4]。目前，临床认为第二种因素是脑梗死神经系统损伤的主要原因，并且认为神经生长抑制因子Nogo-A在其中扮演...