INVESTIGADORES
QUINTEROS Daniela Alejandra
congresos y reuniones científicas
Título:
Desarrollo de modelo animal citotóxico para el tratamiento del glaucoma. Ensayos preliminares.
Autor/es:
BESSONE CAROLINA; CARPENTIERI AGATA; HUGO DIAZ; PALMA SANTIAGO; ALLEMANDI D A.; DANIELA QUINTEROS
Lugar:
ROSARIO
Reunión:
Congreso; Ricifa 2016. Reunión internacional de ciencias farmaceuticas; 2016
Institución organizadora:
RICIFA
Resumen:
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 (ME), 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 developing an animal model where apoptosis trigger mechanism by glutamate (GLUT) and L-buthionine-S, R-sulfoximine (BSO) administration, which causes cytotoxicity and oxidative stress, respectively.To evaluate the function and survival of RGCs, we used electroretinography (ERG) method to evaluate in vivo RCGs function, and histological sections of retina, where we see how many and what types of cells were affected. Additional, immunohistochemical assays are performed to evaluate the death process RGCs, analyzed by optical microscope. The results showed that at high doses of the treatment (200 mM GLUT + 75 mM BSO), a large rate of death of RGCs occur with a decrease in cells of the intermediate surface layer, into a period of 48 hs. While at low doses (200 µM GLUT + 75 µM BSO), to a lesser degree of death of RGCs in a period of 8-15 days, was observed. 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.Reference: 1.Robert W. Nickells. From ocular hypertension to ganglion cell death: a theoretical sequence of events leading to glaucoma. Can J Ophthalmol. 2007; 42:278-87.2.Per O. Lundmark, S.R. Pandi-Perumal, V. Srinivasan, D.P. Cardinali, R.E. Rosenstein. Melatonin in the eye: Implications for glaucoma. Experimental Eye Research. 2006; 84:1021-1030.
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