大鼠视神经挫伤致视网膜硫化氢合成酶表达变化 .pdfVIP

大鼠视神经挫伤致视网膜硫化氢合成酶表达变化

曾铭伟;王涛;费成平;邹彩霞;刘夷嫦;谷振勇

【摘要】目的探讨大鼠视神经挫伤后视网膜硫化氢合成酶胱硫醚γ-裂解酶

(cystathionineγ-lyase,CSE)、胱硫醚β-合成酶(cystathionineβ-synthase,CBS)

和3-巯基丙酮酸硫基转移酶(3-mercaptopyruvatesulfurtransferase,3-MST)的

表达变化.方法建立大鼠视神经挫伤模型.将大鼠分为正常对照组、视神经挫伤组和

假手术组.观察大鼠视网膜的组织病理学变化,检测视网膜神经节细胞数量和视网膜

内侧部分厚度.用实时荧光定量PCR技术检测CBS、CSE和3-MST的mRNA表

达变化.结果正常对照组大鼠视网膜组织结构正常,假手术组仅有轻微变化.与假手

术组比较,视神经挫伤后各组大鼠视网膜出现明显损伤,视网膜神经节细胞数量呈时

间依赖性减少且视网膜内侧部分厚度呈进行性变薄.正常对照组大鼠视网膜存在

CSE、CBS和3-MSTmRNA的基础表达.与正常对照组比较,假手术组CSE、CBS

和3-MST的mRNA表达无明显变化.与假手术组比较,CBSmRNA表达在视神经

挫伤后3d、7d和14d呈时间依赖性上调;CSEmRNA表达在伤后7d达到峰

值,14d时有所下降;3-MSTmRNA表达在视神经挫伤后3d和7d有上调的趋

势,14d时有明显上调.结论大鼠视神经挫伤后视网膜硫化氢合成酶CBS、CSE和

3-MST表达上调,这可能引起视网膜局部内源性硫化氢生成增多并产生代偿性保护

效应.%ObjectiveToinvestigatetheexpressionchangesofthehydrogen

sulfidesynthasescystathionineγ-lyase(CSE),cystathionineβ-synthase(CBS),

and3-mercaptopyruvatesulfurtransferase(3-MST),afteropticnervecrush

(ONC)inrattheretina.MethodsTheratmodelofONCwas

established.Ratsweredividedintonormalcontrol,ONC,andshamcontrol

groups.Histopathologicchangesinretina,thenumberofretinalganglion

cells(RGC)andretinalthicknessofinnerpart(RTIP)weremeasured.The

changesofCSE,CBSand3-MSTmRNAexpressionweredetectedwith

quantitativereal-timePCR.ResultsTheretinalhistostructurewasnormalin

normalcontrolsandwithminorchangesinshamcontrols,

respectively.Comparedwithshamgroup,significantretinadamageswere

foundintheONCgroup:atime-dependentreductionofRGCnumberand

RTIP.ExpressionsofCSE,CBSand3-MSTmRNAinratretinaweredetected

innormalcontrol.Comparedwithnormalcontrols,theexpressionsofCSE,

CBSand3-MSTmRNAdidnotshowanysignificantchangesinthesham

controls.Comparedwithshamcontrols,CBSmRNAexpressionsshoweda

time-dependentincreaseat3d