<![CDATA[Optic neuritis (ON) is an idiopathic inflammatory demyelinating condition of the optic nerve, vulnerable to degeneration due to energy depletion, reactive oxygen species (ROS) accumulation, and mitochondrial dysfunction. Superoxide dismutase (SOD) may offer neuroprotective benefits by targeting redox dysregulation, helping to halt retinal and retinal ganglion cell (RGC) degeneration. When combined with methylprednisolone (MP), which reduces inflammation, this therapy may accelerate recovery and minimize optic nerve damage. The ASK1-p38 pathway further supports this combined mechanism. To evaluate the effects of SOD and MP administration on optic nerve damage in a rat model of optic neuritis. This randomized post-test only control group laboratory experiment involved 35 male Wistar rats allocated into five groups: sham, control, SOD, MP, and combination therapy. Optic neuritis was induced by lipopolysaccharide (LPS) injection into the optic nerve. Histopathological data were collected after 14 days of treatment through microscopic evaluation of retinal ganglion cell (RGC) counts, optic nerve edema, demyelination, and hemorrhage. Data were analyzed using One-Way ANOVA or Kruskal-Wallis tests. The combination group demonstrated the most favorable outcomes, with the highest average RGC count (195 cells), minimal optic nerve edema (p<0.001), and demyelination levels similar to normal. Combined administration of SOD and MP provided better histopathological outcomes—reflected in ganglion cell preservation, reduced edema, and minimal demyelination—than either treatment alone in this rat model of optic neuritis.]]>
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