Abstract
BackgroundA 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.MethodsPhotodynamic 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.ResultsAfter 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/mm2 and 2078 ± 141/mm2 (p < 0.01), respectively.ConclusionsVerteporfin 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.
Highlights
Anterior ischemic optic neuropathy (AION) is the leading cause of sudden optic nerve-related (ON-related) vision loss in elderly people
AION is considered a secondary symptom to ischemia, which is predominantly caused by the posterior ciliary arteries [3], the exact pathophysiology that leads to axonal degeneration remains undiscovered
In the photodynamically treated eyes, Fundus Fluorescein angiography (FFA) indicated fluorescein leakage from the optic nerve head (ONH) vasculature on day 1, (Fig. 1b, c) which was consistent with the swelling of the retina tissue as demonstrated by the spectral domain optical coherence tomography (SD-OCT) images
Summary
Anterior ischemic optic neuropathy (AION) is the leading cause of sudden optic nerve-related (ON-related) vision loss in elderly people. AION was notably noted in one eye, according to a previous study conducted in China, with an incidence rate of 0.03+/− 0.03% (mean +/− standard error) per 5 years (1:16,000 subjects annually) [2]. AION is considered a secondary symptom to ischemia, which is predominantly caused by the posterior ciliary arteries [3], the exact pathophysiology that leads to axonal degeneration remains undiscovered. To date no effective method has been reported to prevent vision loss following the development of AION. It is necessary to establish an animal model of AION that can be used to assess the potential benefits of neuroprotective strategies. The analysis of the morphological function, the pathological changes and the potential mechanism of action were further investigated
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