Nutraceutical Supplementation Ameliorates Visual Function, Retinal Degeneration, and Redox Status in rd10 Mice.

Lorena Olivares-González,José Miguel Soriano Del Castillo,David Salom,Sheyla Velasco,Emilio González-García,Isabel Campillo,Regina Rodrigo

doi:10.3390/antiox10071033

Abstract

Retinitis pigmentosa (RP) is a group of inherited retinal dystrophies characterized by progressive degeneration of photoreceptor cells. Ocular redox status is altered in RP suggesting oxidative stress could contribute to their progression. In this study, we investigated the effect of a mixture of nutraceuticals with antioxidant properties (NUT) on retinal degeneration in rd10 mice, a model of RP. NUT was orally administered to rd10 mice from postnatal day (PD) 9 to PD18. At PD18 retinal function and morphology were examined by electroretinography (ERG) and histology including TUNEL assay, immunolabeling of microglia, Müller cells, and poly ADP ribose polymers. Retinal redox status was determined by measuring the activity of antioxidant enzymes and some oxidative stress markers. Gene expression of the cytokines IL-6, TNFα, and IL-1β was assessed by real-time PCR. NUT treatment delayed the loss of photoreceptors in rd10 mice partially preserving their electrical responses to light stimuli. Moreover, it ameliorated redox status and reduced inflammation including microglia activation, upregulation of cytokines, reactive gliosis, and PARP overactivation. NUT ameliorated retinal functionality and morphology at early stages of RP in rd10 mice. This formulation could be useful as a neuroprotective approach for patients with RP in the future.

Highlights

Retinitis pigmentosa (RP) is a group of inherited retinal disorders characterized by progressive degeneration of photoreceptors, which eventually leads to blindness
We previously reported the first peak of photoreceptor degeneration and an altered antioxidant response in rd10 retinas at PD18 [10,11]
We showed that nutraceuticals with antioxidant properties (NUT) supplementation reduced microglial activation, IL-6, IL-1β, and to a lesser degree TNFα upregulation

Summary

Introduction

Retinitis pigmentosa (RP) is a group of inherited retinal disorders characterized by progressive degeneration of photoreceptors (rods and cones), which eventually leads to blindness. It is a rare disease with a prevalence of approximately 1 in 4.000 individuals [1]. Patients with RP usually lose night vision and peripheral vision in the early stages of the disease, and eventually, central vision. The vision loss is mainly due to a gradual deterioration of photoreceptor cells, namely, rod degeneration, which is responsible for night and peripheral vision, followed by cone degeneration responsible for central and color vision. Genetic mutations affect rod survival but eventually promote cone degeneration. Evidence indicates that rod degeneration triggers the release and accumulation of free radicals, inflammatory molecules, etc. that eventually would affect cone survival [2]

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