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Protective role of melatonin on retinal ganglionar cell: In vitro an in vivo evidences
- del Valle Bessone, Carolina, Fajreldines, Hugo Diaz, de Barboza, Gabriela Edit Diaz, Tolosa de Talamoni, Nori Graciela, Allemandi, Daniel Alberto, Carpentieri, Agata Rita, Quinteros, Daniela Alejandra
- Life sciences 2019 v.218 pp. 233-240
- apoptosis, autophagy, axons, cytotoxicity, death, ganglia, glaucoma, immunohistochemistry, macular degeneration, melatonin, models, necrosis, nerve tissue, neurodegenerative diseases, nitrogen, oxidants, oxidative stress, protective effect, reactive oxygen species, therapeutics
- 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.