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ID:15161925
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页数:8页
时间:2018-08-01
《大鼠慢性高眼压视网膜nogoa的表达》由会员上传分享,免费在线阅读,更多相关内容在学术论文-天天文库。
1、大鼠慢性高眼压视网膜NogoA的表达作者:聂庆珠,刘致力,沙倩,高殿文【摘要】 目的:研究慢性高眼压大鼠视网膜髓鞘相关抑制蛋白NogoA表达的变化。方法:成年雄性Wistar大鼠36只随机分为正常对照组6只和慢性高眼压组30只,应用免疫组织化学方法观察慢性高眼压大鼠视网膜不同时点NogoA表达的变化。结果:与正常对照组相比,慢性高眼压21d大鼠视网膜变薄,节细胞数量减少(P<0.05);NogoA表达增多,与形态学变化相一致(P<0.05)。结论:髓鞘相关抑制蛋白NogoA在慢性高眼压大鼠视网膜损伤过程中发挥了重要作用。【
2、关键词】视网膜;慢性高眼压;NogoA;视网膜神经节细胞 AbstractAIM:TostudytheexpressivevariationofNogoAonratretinaintheprocessofchronicocularhypertension.METHODS:ThirtysixhealthyadultmaleWistarswererandomlydividedintocontrolgroup(6rats)andchronichypertensiongroup(30rats).Chronichypertensionwascre
3、atedbycauterizingthesuperficialscleralveins.8ImmunohistochemistrytechniquewasusedtoevaluatetheexpressivevarietiesofNogoAatdifferenttimepointsduringthecourseofchronicocularhypertension.RESULTS:Thesuccessofthemodelwasindicatedbyover40%ofincreaseintheIOPascomparedwithnormalrats
4、.Comparedwithcontrolgroup,astimepassedchronichypertensiongroupgraduallyhaddetectablemorphologychangesintheretina.Atthe21stdayofchronicocularhypertension,retinasbecamethinnerandthequantityofretinalganglioncell(RGC)decreased(P<0.05).Assoicatedwiththemorphologicalchanges,thee
5、xpressionofNogoAwasstronglyincreased(P<0.05).CONCLUSION:MyelinassociatedproteinNogoAplaysapartintheprocessofchronicocularhypertension. KEYWORDS:retina;chronichypertension;NogoA;retinalganglioncell INTRODUCTION Thepathologicalmechanismofglaucomatousopticneuropathyispr
6、ogressivedeathofretinalganglioncells,whichleadstoirreversibledamage.Regenerationofdamagedcentral8nervoussystem,includingopticnerve,isdifficulttoachievebecauseofanumberofreasons,suchasinhibitorsofaxonalregenerationarepresentinmyelin,lackofneurotrophicfactors,andformationoftheg
7、liascar.IthasbeenpostulatedthattheregenerationofcentralnervoussystemisaffectedbymyelinassociatedproteinNogoA.NogoA,whichispredominantlypresentinoligodendrocytesandmyelinintheadultcentralnervoussystem(CNS),notonlyrestrictsneuritegrowth,plasticity,andaxonalregeneration,butals
8、olimitstheinvasionandmigrationofcellsandtumorsintheCNS[1].Therefore,
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