Evaluation and Application of a Rat Model of Ischemic Ophthalmopathy
Objective:To evaluate the pathological characteristics and application of rat models of mild and severe ischemic ophthalmopathy induced by electrocoagulation.Methods:Anisodine hydrobromide was used to evaluate the rat models of different degrees of thrombotic ischemic oph-thalmopathy.Rats were randomized into the sham control,mild model control,anisodine hydrobromide Ⅰ(0.045 mg/kg),severe model con-trol,and anisodine hydrobromide Ⅱ(0.045 mg/kg)groups.Rats were administrated with corresponding drugs by gavage for 28 consecutive days.The changes of blood vessels and microvessels in the ocular tissue were observed by iris photographing,fundus retinal microimaging,and periodic acid-Schiff staining.The changes of ocular tissue structure were observed by optical coherence tomography and hematoxylin-eosin staining.Oximetry was employed to compare the blood oxygen level in the ocular tissue between groups.Visual electrophysiology was adopted to reveal the visual function changes.The immunohistochemical assay was used to detect the positive expression of rhodopsin(RHO),clau-din-5,and glial fibrillary acidic protein(GFAP).Results:Compared with the sham control group,the two model control groups showed differ-ent degrees of ischemia and flow disruption in the iris,retina,choroidal vessels and retinal microvessels as well as structural changes of the ret-ina and choroid.The mild model control group presented no significant changes in the thickness of the corneal epithelial layer and the corneal thickness,lens,and optic nerves.However,the severe model group presented corneal epithelial cell atrophy,changed corneal thickness and corneal epithelial layer thickness(P＜0.01),deformed mesenchymal cells,lost,deformed,and disarranged epithelial cells in the lens,and pro-liferated and disarranged glial cells of the optic nerve(P＜0.01).The two model groups had lower blood oxygen saturation and perfusion in-dex than the other groups(P＜0.01).In terms of the visual function,the amplitudes of the rod cell response,maximal mixed response,oscilla-tory potential response,the cone cell response,and the 20-HZ scintillation response decreased in the two model groups(P＜0.05 or P＜0.01).In addition,the two model groups showed down-regulated protein levels of RHO and claudin-5 and up-regulated protein level of GFAP(P＜0.05 or P＜0.01).Compared with the mild and severe model control groups,the anisodine hydrobromide Ⅰ and Ⅱ groups showed signifi-cant differences in the above indicators(P＜0.05 or P＜0.01).Conclusion:Mild ocular ischemia is manifested by ischemia of the iris,reti-na,and choroid,and severe ocular ischemia presents ischemia of the cornea,lens,and optic nerve additionally.Anisodine hydrobromide can repair the ocular ischemia-induced damage of ocular blood vessels,ocular tissue structure(especially optic nerves),and retinal photoreceptor cells and improve the ocular blood oxygen level,thereby maintaining the visual function.The findings provide a reference for the application of animal models of different degrees of ischemic ophthalmopathy and the drug evaluation.
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