Min Jing-Yu, Lv Yanan, Mao Lei, Gong Yuan-Yuan, Gu Qing, Wei Fang
Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, NO.100, Haining Road, Hongkou District, Shanghai, 200080, China.
Shanghai Key Laboratory of Ocular Fundus Diseases, NO.100, Haining Road, Hongkou District, Shanghai, 200080, China.
BMC Ophthalmol. 2018 Nov 22;18(1):304. doi: 10.1186/s12886-018-0937-5.
A rodent model of photodynamic AION resulting from intravenous verteporfin is presented. The analysis of the morphological function, the pathological changes and the potential mechanism of action were further investigated.
Photodynamic treatment was conducted on the optic nerve head (ONH) following administration of the photosensitizer. The fellow eye was considered as sham control. Fundus Fluorescein angiography (FFA), spectral domain optical coherence tomography (SD-OCT) and Flash-visual evoked potential (F-VEP) recordings were conducted at different time points. Immunohistochemistry was used to observe apoptotic cell death (TUNEL) and macrophage infiltration (ED-1/Iba-1). Retrograde labeling of retinal ganglion cells (RGCs) was used to evaluate the loss of RGCs.
After laser treatment, SD-OCT indicated optic nerve edema, while FFA indicated late leakage of the ONH. F-VEPs were distinctly reduced compared to control eyes. The number of apoptotic RGCs peaked on day 14 (5.71 ± 0.76, p < 0.01). The infiltration of ED-1 and Iba-1 increased on the 3rd day following PDT, while it peaked on day 14 (67.5 ± 9.57 and 77.5 ± 12.58 respectively, p < 0.01). Following 3 weeks of AION, the densities of RGCs in the central retinas of the normal and AION eyes were 3075 ± 298/mm and 2078 ± 141/mm (p < 0.01), respectively.
Verteporfin photodynamic treatment on rodents ONH can lead to functional, histological, and pathological changes. This type of animal model of AION is easy to establish and stable. It can be used for studying the mechanism and neuroprotective medicine of AION injury.
提出了一种由静脉注射维替泊芬引起的光动力性前部缺血性视神经病变（AION）的啮齿动物模型。进一步研究了其形态功能、病理变化及潜在作用机制。
在给予光敏剂后，对视神经乳头（ONH）进行光动力治疗。对侧眼作为假对照。在不同时间点进行眼底荧光血管造影（FFA）、光谱域光学相干断层扫描（SD-OCT）和闪光视觉诱发电位（F-VEP）记录。采用免疫组织化学法观察凋亡细胞死亡（TUNEL）和巨噬细胞浸润（ED-1/Iba-1）。利用视网膜神经节细胞（RGCs）的逆行标记来评估RGCs的损失。
激光治疗后，SD-OCT显示视神经水肿，而FFA显示ONH晚期渗漏。与对照眼相比，F-VEP明显降低。凋亡RGCs数量在第14天达到峰值（5.71±0.76，p<0.01）。PDT后第3天ED-1和Iba-1的浸润增加，而在第14天达到峰值（分别为67.5±9.57和77.5±12.58，p<0.01）。AION发生3周后，正常眼和AION眼中央视网膜RGCs的密度分别为3075±298/mm和2078±141/mm（p<0.01）。
维替泊芬光动力治疗啮齿动物ONH可导致功能、组织学和病理学改变。这种AION动物模型易于建立且稳定。可用于研究AION损伤的机制和神经保护药物。
