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Research Article: Local delivery of nerve growth factor in traumatic optic neuropathy: neuroprotective effects in a rat model

Date Published: 2026-05-01

Abstract:
In the present study, we established a rat model of optic nerve injury to evaluate whether direct local delivery of neurotrophic agents following traumatic optic neuropathy (TON) enhances retinal ganglion cells (RGCs) survival and its potential effects on axonal regeneration. Forty-eight rats were randomly assigned to treatment ( n =?24) and control ( n =?24) groups. A standardized optic nerve crush injury was induced, followed by optic nerve decompression. In the treatment group, a gelatin sponge soaked with 10-?L mouse NGF (mNGF) solution was applied directly to the injury site. In the control group, a gelatin sponge soaked with 10-?L normal saline was applied. Retinal structure and cellular changes were evaluated via hematoxylin–eosin (H&E) staining at postoperative days 1, 8, and 14. RGC survival was quantified via immunofluorescence staining. Axonal survival was assessed using cholera toxin B subunit–488 (CTB-488) anterograde tracing. Compared with the control group, H&E staining showed better preservation of retinal morphology in the mNGF-treated group. CTB-488 anterograde tracing showed no significant differences between groups in mean axonal fluorescence intensity at the injury site. Immunofluorescence analysis revealed significantly higher RGC survival in the treatment group at days 1 (1/2 retinal eccentricity), 8 (1/6 and 1/2 eccentricities), and 14 (1/6 eccentricity). In this Sprague–Dawley rat model of optic nerve injury, direct local delivery of mNGF may enhance RGC survival with effects showing time-dependent and spatially heterogeneous patterns. However, this intervention does not significantly promote the survival or regeneration of optic nerve axons.

Introduction:
Traumatic optic neuropathy (TON) is a common form of ocular trauma, typically resulting from blunt impact to the superolateral orbital region involving the frontal or temporal areas. It is also a severe complication of closed head injury. TON incidence has been increasing annually, and 68–78% of patients present with no light perception immediately after trauma ( 1 ). Currently, three principal treatment strategies are available, namely conservative management, corticosteroid therapy, and surgical decompression (…

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