Animal model for the study of neuroprotective treatment of glaucoma. Preliminary studies.

BESSONE CAROLINA; CARPENTIERI AGATA; DIAZ HUGO; PALMA SANTIAGO; ALLEMANDI DANIEL; QUINTEROS DANIELA

Rosario, Santa Fe

Congreso; 4º Reunión Internacional de Ciencias Farmacéuticas (RICiFa); 2016

Facultad de Ciencias Bioquímicas y Farmacéuticas, UNR - Facultad de Ciencias Químicas, UNC.

Glaucoma is the leading cause of irreversible blindness worldwide and is characterized by progressive optic nerve degeneration and death of the retinal ganglion cell (RGC) (1). Reducing intraocular pressure (IOP) by drugs and/or surgery is the standard treatment. However, it is not always effective; even after the success in reducing the IOP. Therefore, alternative treatments, for example, neuroprotection, have long been sought. Preliminary studies showed that melatonin, a neurohormone that is synthesized in paracrine manner on the retina, exerts an antiapoptotic neuroprotective effect on RGCs in cultura, added to which comply hypotensive functions (2).To investigate the neuroprotective efficacy of ME on RGCs in rabbit models of glaucoma, we are in the process of development of an animal model where apoptotic trigger mechanism by administration of doses of glutamate (GLUT) and L-buthionine-S, R-sulfoximine (BSO), which causes oxidative stress and cytotoxicity.For this, the state of RGCs at different doses was evaluated by electroretinography (ERG) to evaluate in vivo RCGs function, and histological sections of retina, where we see how many and what types of cells were affected. The results shown that at high doses (200 mM GLUT + 75 mM BSO), a high proportion of death of RGCs and a decrease in cells of the intermediate and surface layer, into a period of 48 hs. While at low doses (200 µM GLUT + 75 µM BSO), was observed to a lesser degree and in a period of 8-15 days. Our next challenge is to incorporate ME during the process of apoptosis and to demonstrate the neuroprotective effect, slowing or reversing the process of cell death.