Exploring minocyclines effect on retinal degeneration following N-methyl-N-nitrosourea exposure in rats

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Retinal degeneration (RD) isoften associated with deficiencies orthe inaccurate production ofphotoreceptor-specific proteins, which are encoded byvarious genes and characterised bythe apoptotic and ongoing death ofphotoreceptor cells. This study involved administering asingle intraperitoneal (i.p.) dose of50mg/kg ofN-methyl-N-nitrosourea (MNU) torats toinduce RD. Some ofthese rats also received intraperitoneal minocycline atvarying doses toprevent RD. Euthanasia was conducted atfive intervals: at12, 24, 48, and 72h, and onthe7thday; and eye samples were taken. These samples were analysed using histopathology, immunohistochemistry, and electron microscopy. Significant RD was observed inthe MNU-treated groups, with photoreceptor cell apoptosis demonstrated bythe TUNEL method. Compared with those inthe control group, there was aprogressive thinning ofthe photoreceptor layer and outer nuclear layer, along with increased levels ofglial fibrillary acidic protein (GFAP) and proliferating cell nuclear antigen (PCNA), and reduced levels ofrhodopsin and red/green opsin starting from the 12thhour in the experimental groups. Electron microscopy revealed that amacrine and bipolar cells, in addition to photoreceptors, were also affected. The minocycline treatment did not show significant differences in retinal layer thickness or the staining levels of PCNA, GFAP, and opsins in the MNU-induced RD model.