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一种新的视网膜脱离实验小鼠模型:视网膜的完全功能和组织学恢复。

A novel experimental mouse model of retinal detachment: complete functional and histologic recovery of the retina.

机构信息

Eye Hospital, School of Ophthalmology and Optometry, Wenzhou Medical College, Wenzhou, People’s Republic of China.

出版信息

Invest Ophthalmol Vis Sci. 2012 Mar 26;53(3):1685-95. doi: 10.1167/iovs.11-8241.

Abstract

PURPOSE

To establish an experimental mouse model of retinal detachment (RD) created by corneal puncture (CP).

METHODS

Mouse corneas were punctured with a 30.5-gauge beveled needle, and the anterior chamber was penetrated. Histologic and functional changes of the retina were examined by light microscopy and electroretinography (ERG). Certain retinal cellular responses were examined by immunofluorescence microscopy. Internucleosomal DNA fragmentation in the retina was determined by terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick-end labeling (TUNEL). RESULTS. CP caused transient leakage of aqueous humor along the needle shaft and immediate formation of multiple retinal blebs, which shrank and flattened within 24 hours. Bleb formation was associated with detachment of the neuroretina from the retinal pigment epithelium (RPE). After CP, the RPE cells underwent extensive transformation during retinal detachment/reattachment, but they resumed normal morphology on retinal reattachment around 10 to 13 days after CP. Relative to pre-CP ERG amplitudes, the punctured eyes showed decreases of 45% and 24% in scotopic and 7% and 12% in photopic b- and a-wave amplitudes, respectively, within 10 to 20 minutes after CP. The ERG amplitudes recovered fully by 12 hours after CP. No infiltrated cells were observed in the subretinal space, and no proliferating or TUNEL-positive cells were observed in the retina of the punctured eyes.

CONCLUSIONS

Puncturing the mouse cornea can create transient RD, and the functional and histologic changes in the retina can subsequently recover. This experimental mouse model of RD mimics human traction and serous RD.

摘要

目的

建立通过角膜穿刺(CP)诱导的视网膜脱离(RD)实验性小鼠模型。

方法

使用 30.5 号斜面针穿刺小鼠角膜,穿透前房。通过光镜和视网膜电图(ERG)检查视网膜的组织学和功能变化。通过免疫荧光显微镜检查某些视网膜细胞反应。通过末端脱氧核苷酸转移酶介导的尿嘧啶 5'-三磷酸生物素缺口末端标记(TUNEL)测定视网膜内核小体 DNA 片段化。

结果

CP 导致沿针轴的房水短暂漏出,并立即形成多个视网膜泡,这些泡在 24 小时内缩小和平坦化。泡的形成与神经视网膜从视网膜色素上皮(RPE)分离有关。CP 后,RPE 细胞在视网膜脱离/再附着期间经历了广泛的转化,但在 CP 后约 10 至 13 天视网膜再附着时恢复正常形态。与 CP 前 ERG 幅度相比,穿刺眼在 CP 后 10 至 20 分钟内,暗视野和光视野 b-和 a 波幅度分别下降 45%和 24%以及 7%和 12%。CP 后 12 小时 ERG 幅度完全恢复。在穿刺眼的视网膜下间隙未观察到浸润细胞,也未观察到增殖或 TUNEL 阳性细胞。

结论

穿刺小鼠角膜可引起短暂性 RD,随后视网膜的功能和组织学变化可恢复。这种实验性 RD 小鼠模型模拟了人类牵引性和浆液性 RD。

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