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To investigate the neuroprotective effects of the mitochondria-targeted antioxidant Szeto-Schiller peptide 31 (SS-31) in a rat experimental glaucoma model,SS-31 was intraperitoneally (IP) injected into Sprague-Dawley rats,followed by intracameral injection of polystyrene microspheres to induce elevated intraocular pressure (IOP).After 6 weeks,electroretinography (ERG) and flash visual-evoked potentials (F-VEPs) were recorded to assess retinal function.Hematoxylin-eosin staining was performed on retinal cross-sections to measure ganglion cell complex (GCC) thickness.Apoptotic retinal cells were assessed by TUNEL staining.B3a-positive retinal ganglion cells (RGCs) were counted in retinal flat mounts via immunofluorescence.The retinal total SOD,SOD2,and MDA expression levels were assessed in retinal tissue homogenates.The cyt c,Bax,and Bcl-2 protein levels in rat retinas were detected by weste blot analysis.Bax and Bcl-2 expressions were also evaluated using immunohistochemistry in paraffinized sections.Our results showed that the rats that received microsphere injection developed elevated lOP.SS-31 ameliorated the reductions in the a-and b-wave amplitudes on ERG and the F-VEP amplitude in glaucomatous eyes.GCC thickness was preserved,TUNEL-positive cells were decreased in the retina,and B3a-positive RGCs were increased in the SS-31-treated glaucoma group compared with those in the non-treated glaucoma group.SS-31 significantly reduced MDA levels and increased SOD2 levels after glaucoma induction.Significant suppression of cyt c release,upregulation of Bcl-2,and downregulation of Bax were observed following SS-31 administration.In summary,SS-31 exerts neuroprotective effects in this experimental glaucoma model by inhibiting mitochondrial dysfunction and therefore represents a promising therapeutic agent for glaucoma.