Protective role of melatonin on retinal ganglionar cell: In vitro an in vivo evidences.

Autor: Del Valle Bessone C; Unidad de Investigación y Desarrollo en Tecnología Farmacéutica (UNITEFA), CONICET and Departamento de Ciencias Farmacéuticas, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Ciudad Universitaria, 5000 Córdoba, Argentina., Fajreldines HD; Laboratorio de Neurofisiología, Instituto de Neurociencias Córdoba, 5000 Córdoba, Argentina., de Barboza GED; Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, INICSA/CONICET-UNC, Argentina., Tolosa de Talamoni NG; Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, INICSA/CONICET-UNC, Argentina., Allemandi DA; Unidad de Investigación y Desarrollo en Tecnología Farmacéutica (UNITEFA), CONICET and Departamento de Ciencias Farmacéuticas, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Ciudad Universitaria, 5000 Córdoba, Argentina., Carpentieri AR; Instituto de Investigación en Ciencias de la Salud (INICSA)/CONICET, Universidad Nacional de Córdoba and Cátedra B de Química Biológica, Facultad de Odontología, Universidad Nacional de Córdoba, Ciudad Universitaria, Argentina. Electronic address: agata.carpentieri@unc.edu.ar., Quinteros DA; Unidad de Investigación y Desarrollo en Tecnología Farmacéutica (UNITEFA), CONICET and Departamento de Ciencias Farmacéuticas, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Ciudad Universitaria, 5000 Córdoba, Argentina. Electronic address: danielaq@fcq.unc.edu.ar.
Jazyk: angličtina
Zdroj: Life sciences [Life Sci] 2019 Feb 01; Vol. 218, pp. 233-240. Date of Electronic Publication: 2018 Dec 31.
DOI: 10.1016/j.lfs.2018.12.053
Abstrakt: Oxidative stress triggers ocular neurodegenerative diseases, such as glaucoma or macular degeneration. The increase of reactive oxygen and nitrogen species in retinal ganglion cells (RGCs) causes damage to the structure and function of the axons that make up the optic nerve, leading to cell death arising from apoptosis, necrosis or autophagy in the RCGs. The use of antioxidants to prevent visual neurodegenerative pathologies is a novel and possibly valuable therapeutic strategy. To investigate in vitro and in vivo neuroprotective efficacy of melatonin (MEL) in RGCs, we used a model of oxidative glutamate (GLUT) toxicity in combination with l-butionin-S, R-sulfoximine (BSO), which induces cell death by apoptosis through cytotoxicity and oxidative stress mechanisms. Histological sectioning and immunohistochemical assays using the TUNEL technique were performed to determine the damage generated in affected cells and to observe the death process of RGCs. Whit BSO-GLUT the results revealed a progressive RGCs death without any significant evidence of a decreased retinal function after 9 days of treatment. In this way, we were able to develop a retinal degeneration model in vivo to carry out treatment with MEL and observed an increase in the survival percentage of RGCs, showing that BSO-GLUT could not exert an oxidant effect on cells to counteract the effect of MEL. These findings reveal that MEL has a neuroprotective and antiapoptotic effect as evidenced by the reduction of oxidative stress damage. MEL demonstrated in this model makes it a promising neuroprotective agent for the treatment of ocular neurodegenerative diseases when administered locally.
(Copyright © 2019 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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