Abstract
Retinitis pigmentosa (RP) is a group of inherited retinopathies characterized by photoreceptors death. Our group has shown the positive progesterone (P4) actions on cell death progression in an experimental model of RP. In an effort to enhance the beneficial effects of P4, the aim of this study was to combine P4 treatment with an antioxidant [lipoic acid (LA)] in the rd1 mice. rd1 and control mice were treated with 100 mg/kg body weight of P4, LA, or a combination of both on postnatal day 7 (PN7), 9, and 11, and were sacrificed at PN11. The administration of LA and/or P4 diminishes cell death in rd1 retinas. The effect obtained after the combined administration of LA and P4 is higher than the one obtained with LA or P4 alone. The three treatments decreased GFAP staining, however, in the far peripheral retina, and the two treatments that offered better results were LA and LA plus P4. LA or LA plus P4 increased retinal glutathione (GSH) concentration in the rd1 mice. Although LA and P4 are able to protect photoreceptors from death in rd1 mice retinas, a better effectiveness is achieved when administering LA and P4 at the same time.
Highlights
Retinitis pigmentosa (RP) is a group of inherited retinopathies characterized by progressive photoreceptor death (Farrar et al, 2002; Daiger et al, 2013)
In an effort to enhance the beneficial effects of P4, the aims of this study were to combine P4 treatment with a widely known and effective antioxidant [α-lipoic acid (LA)], in order to increase the antioxidant properties of our treatment, and to establish the changes induced by this combined treatment in the retina of rd1 mice
All groups of rd1 mice showed an increment in the number of transferase dUTP nick end labelling (TUNEL)-positive cells when compared with their respective control groups (∗p < 0.02 vs. control groups)
Summary
Retinitis pigmentosa (RP) is a group of inherited retinopathies characterized by progressive photoreceptor death (Farrar et al, 2002; Daiger et al, 2013). RP accounts for approximately half of the cases of hereditary retinal diseases worldwide (Daiger et al, 2013). More than 100 genes have been linked to RP, the exact mechanisms underlying this retinal degeneration that lead to photoreceptor death remain controversial. Some retinal changes result as a direct mutation effect, some other changes result from modifications of the transcriptional system (Sancho-Pelluz et al, 2008). A substantial body of data suggests that increase oxidative stress, alterations in the inflammatory response, and retinal remodeling play a crucial role in RP pathogenesis (Sanz et al, 2007; Noailles et al, 2014; Jones et al, 2016; Sánchez-Vallejo et al, 2016)
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