Protective effects of quercetin in a rodent model of anterior ischemic optic neuropathy (rAION)

Abstract Background: Anterior ischemic optic neuropathy (AION) is the leading cause of sudden optic nerve-related (ON-related) vision loss in elderly people. However, no considerable treatments are available for the neuroprotection of NAION. The purpose of this study was to detect the effects of intravitreal injection of quercetin (Qcn) in a rodent model of anterior ischemic optic neuropathy (rAION). Methods: The rAION model was established using verteporfin and laser in a photodynamic procedure on the optic discs (ON) of rats. The rats received intravitreal injection of Qcn 2 days before the injury and once/week for 4 weeks after the infarct on optic neuropathy. Flash-visual evoked potential (VEP) were recorded to assess the visual function. TUNEL and retrograde Fluorogold labeling assessed the apoptosis and density of retinal ganglion cells (RGCs). ED-1 and Iba-1 staining of the optic nerves displayed the inflammatory response. Results: At 14 days post-infarct, Qcn treatment significantly reduced the number of apoptotic RGCs, as well as, ED1/Iba-1-positive cells/high power field(HPF) in the ON (p<0.01) as compared to the rAION group. At week 4 after rAION, 28.4% VEP amplitudes were estimated in the treated eyes of the fellow eyes in the rAION group and 64.7% in the rAION+Qcn group (p<0.01). In addition, Qcn saved the RGCs in the central retinas as compared to those of the rAION group (1967.5±162.1 and 2868±325.3 mm2, respectively (p<0.01), and the corresponding densities were 1654.8±104.8 and 2208±272.9 mm2 in the mid-peripheral retinas, respectively (p<0.01). Conclusion: The intravitreal injection of Qcn could protect the RGCs from injury in the rAION animal model, as demonstrated anatomically by RGC density and functionally by F-VEP. Moreover, Qcn might exert an anti-apoptosis role in the survival of RGCs and anti-inflammatory in the optic nerves.