CAJ | 학술논문

目的:通过高眼压诱导的视网膜缺血模型和免疫组化方法,探讨parvalbumin(PV),calbindin(CB)和calretinin(CR)三种钙结合蛋白在缺血后视网膜中的表达.方法:24只大鼠(分4组,每组6只)的右眼眼内压升高至14.6 kPa(110 mmHg),维持90 min;左眼作对照.分别存活0,2,7,14 d后处死.其视网膜冷冻切片后,分别作CB、PV和CR的免疫组化反应;邻片用焦油紫染色.结果:在正常视网膜,PV和CB主要表达于内核层;CR表达于内核层、节细胞层和内网层.缺血0 d组中,PV在内核层的表达剧减,而CB和CR仅轻微减少.2 d后,CB和CR明显减少;而PV的表达开始逐渐恢复.至第14天,尽管内核层神经元已减少了1/2,但PV的表达已恢复至正常水平,其阳性神经元与尼氏染色神经元数之比是正常的2倍.同样,相对第7天而言,CB和CR的表达也有一定程度的恢复.结论:PV,CB和CR的阳性神经元对缺血敏感程度不同,且在一定的实验条件下其表达是可逆的.
목적:통과고안압유도적시망막결혈모형화면역조화방법,탐토parvalbumin(PV),calbindin(CB)화calretinin(CR)삼충개결합단백재결혈후시망막중적표체.방법:24지대서(분4조,매조6지)적우안안내압승고지14.6 kPa(110 mmHg),유지90 min;좌안작대조.분별존활0,2,7,14 d후처사.기시망막냉동절편후,분별작CB、PV화CR적면역조화반응;린편용초유자염색.결과:재정상시망막,PV화CB주요표체우내핵층;CR표체우내핵층、절세포층화내망층.결혈0 d조중,PV재내핵층적표체극감,이CB화CR부경미감소.2 d후,CB화CR명현감소;이PV적표체개시축점회복.지제14천,진관내핵층신경원이감소료1/2,단PV적표체이회복지정상수평,기양성신경원여니씨염색신경원수지비시정상적2배.동양,상대제7천이언,CB화CR적표체야유일정정도적회복.결론:PV,CB화CR적양성신경원대결혈민감정도불동,차재일정적실험조건하기표체시가역적.
Objective: To study the changes in the immunoreactivities (ir) of three kinds of calcium binding proteins(CaBPs), parvalbumin (PV), calbindin (CB) and calretinin (CR), in the neurons of the rat retina after ischemia in-duced by intraocular hypertension (IH). Methods: The intraocular pressure of the right eyes of 24 rats was raised to14.6 kPa ( 110 mmHg) for 90 min and the intact left eyes served as controls. The animals were sacrificed after 0 ( immediately), 2, 7 and 14 d survival, respectively, 6 rats in each group. Serial frozen cross sections of the retina were pro-cessed for PV, CB and CR immunohistochemistry and the adjacent series of sections were stained with cresyl violet for cy-toarchitectonic study. Results: In normal retina, PV-ir and CB-ir were observed mainly in the neurons of the inner nucle-ar layer ( INL), and CR-ir was observed in the neurons of the INL and the ganglion cell layer(GCL) and the fibers of theinner plexiform layer (IPL). PV-ir showed a dramatic reduction in INL in the 0 d IH group; and then it showed a progres-sive recovery with survival prolonging, and almost fully recovered in the 14 d IH group (although at meantime the numeri-cal density in INL was only half of that in the control group). CB-ir showed a significant reduction in horizontal cells andan increase in amacrine cells, in 0 d to 7 d IH groups; and a dramatic recovery in 14 d IH group. CR-ir showed an evident reduction in GCL and INL in the 0 d IH group; and further reduction in the 2 d IH group; and then a progressive recovery in the 7 d and 14 d IH groups. Conclusion: PV, CB and CR-containing neurons in the INL and the GCL mightrepresent subpopulation of neurons that were sensitive to ischemia and/or reversible under the exploited experimental condition.