Melatonin protects the retina from experimental non-exudative age-relatd macular degeneration in mice

Abstract: Non-exudative age-related macular degeneration (NE-AMD) represents the leading cause of blindness in the elderly. Currently, there are no available treatments for NE-AMD. We have developed a NE-AMD model induced by superior cervical ganglionectomy (SCGx) in C57BL/6J mice, which reproduces...

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Detalles Bibliográficos
Autores principales: Dieguez, Hernán H., González Fleitas, María F., Aranda, Marcos L., Calanni, Juan S., Keller Sarmiento, María I., Chianelli, Mónica S., Alaimo, Agustina, Sande, Pablo H., Romeo, Horacio E., Rosenstein, Ruth E., Dorfman, Damián
Formato: Artículo
Lenguaje:Inglés
Publicado: John Wiley & Sons 2020
Materias:
MELATONINA
ENFERMEDADES DE LA RETINA
ESTRES OXIDATIVO
CEGUERA
ANTIOXIDANTES
ANCIANOS
TRATAMIENTO MEDICO
Acceso en línea:https://repositorio.uca.edu.ar/handle/123456789/10073
Aporte de:
Repositorio Institucional de la Universidad Católica Argentina (UCA) de Universidad Católica Argentina
Descripción
Sumario:Abstract: Non-exudative age-related macular degeneration (NE-AMD) represents the leading cause of blindness in the elderly. Currently, there are no available treatments for NE-AMD. We have developed a NE-AMD model induced by superior cervical ganglionectomy (SCGx) in C57BL/6J mice, which reproduces the disease hallmarks. Several lines of evidence strongly support the involvement of oxidative stress in NEAMD- induced retinal pigment epithelium (RPE) and outer retina damage. Melatonin is a proven and safe antioxidant. Our aim was analyzing the effect of melatonin in the RPE/outer retina damage within experimental NE-AMD. The treatment with melatonin starting 48 h after SCGx, which had no effect on the ubiquitous choriocapillaris widening, protected visual functions, and avoided Bruch´s membrane thickening, RPE melanin content, melanosome number loss, retinoid isomerohydrolase (RPE65)- immunoreactivity decrease, and RPE and photoreceptor ultrastructural damage induced within experimental NE-AMD exclusively located at the central temporal (but not nasal) region. Melatonin also prevented the increase in outer retina/RPE oxidative stress markers, and a decrease in mitochondrial mass at 6 weeks post-SCGx. Moreover, when the treatment with melatonin started at 4 weeks post-SCGx, it restored visual functions and reversed the decrease in RPE melanin content and RPE65-immunoreactivity. These findings suggest that melatonin could become a promising safe therapeutic strategy for NE-AMD.

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