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时间:2020-04-04
《临床医学毕业论文大鼠慢性高眼压视网膜nogoa的表达.doc》由会员上传分享,免费在线阅读,更多相关内容在工程资料-天天文库。
1、毕业论文大鼠慢性高眼压视网膜NowA的表达名:2014年6月25日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ANogoA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(P0.05);NogoA表达增多,与形态学变化相一致(P0.05)o结论:髓鞘相关抑制蛋ANogoA在慢性高眼
2、压大鼠视网膜损伤过程中发挥了重要作用。【关键词】视网膜;慢性高眼压;NogoA;视网膜神经节细胞AbstractAIM:TostudytheexpressivevariationofNogoAonratretinaintheprocessofchronicocularhypcrtcnsion.METHODS:ThirtysixhealthyadultmaleWistarswererandomlydividedintocontrolgroup(6rats)andchronichypertensiongroup(30rats).Chronichy
3、pertensionwascreatedbycauterizingthesuperficialscleralveins.ImmunohistochemistrytechniquewasusedtoevaluatetheexpressivevarietiesofNogoAatdifferenttimepointsduringthecourseofchronicocularhypertension.RESULTS:Thesuccessofthemodelwasindicatedbyover40%ofincreaseintheIOPascompar
4、edwithnormalrats.Comparedwithcontrolgroup,astimepassedchronichypertensiongroupgraduallyhaddetectablemorphologychangesintheretina.Atthe21stdayofchronicocularhypertension,retinasbecamethinnerandthequantityofretinalganglioncell(RGC)decreased(P0.05).Assoicatedwiththemorphologic
5、alchanges,theexpressionofNogoAwasstronglyincreased(P0.05).CONCLUSION:MyelinassociatedproteinNogoAplaysapartintheprocessofchronicocularhypertension.KEYWORDS:retina;chronichypertension;NogoA;retinalganglioncellINTRODUCTIONThepathologicalmechanismofglaucomatousopticneuropathyi
6、sprogressivedeathofretinalganglioncells,whichleadstoirreversibledamage.Regenerationofdamagedcentralnervoussystem,includingopticnerve,isdifficulttoachievebecauseofanumberofreasons,suchasinhibitorsofaxonalregenerationarcpresentinmyelin,lackofneurotrophicfactors,andformationof
7、thegliasea匚IthasbeenpostulatedthattheregenerationofcentralnervoussystemisaffectedbymyelinassociatedproteinNogoA.NogoA,whichispredominantlypresentinoligodendrocytesandmyelinintheadultcentralnervoussystem(CNS),notonlyrestrictsneuritegrowth,plasticity,andaxonalregeneration,but
8、alsolimitstheinvasionandmigrationofcellsandtumorsintheCNS[1].Therefore,ourfindingo
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