Bacterial lipopolysaccharide-induced protection against light-induced retinal damage in rats.

MELINA BORDONE; FLORENCIA LANZANI; JUAN JOSÉ LÓPEZ; RUTH ROSENSTEIN

Huerta Grande, Córdoba

Congreso; Second Joint Meeting of the Argentine Society for Neuroscience (SAN: XXV Reunión Anual de la Sociedad Argentina de Investigación en Neurociencias) and the Argentine Workshop in Neuroscience (TAN: XII Taller Argentino de Neurociencias); 2010

SAN (Sociedad Argentina de Investigación en Neurociencias) y TAN (Taller Argentino de Neurociencias)

We analyzed the effect of lipopolysaccharide (LPS) on light-induced retinal damage. Male Wistar rats were intravitreously injected with LPS in one eye and vehicle in the fellow eye, one day before an intense light exposure for 24 h. Electroretinograms (ERGs) were registered at several time points after light exposure, and retinal histology was examined 14 days after light. Apoptosis was examined through the assessment of mitochondrial bax/cytosolic bax ratio, and lipid peroxidation was evaluated through the TBARS method. Animals were injected with an iNOS inhibitor (aminoguanidine, AG) or a mitochondrial K+ ATP channel blocker (5-hydroxidecanoic acid, 5HD), or a phosphatidylinositol 3-kinase (PI3K) inhibitor (wortmannin, WT) and electroretinographic and histological analysis were performed 7 days after light exposure. Light significantly decreased the ERG a- and b-wave amplitude, and the total retina, photoreceptor segments, outer nuclear layer thickness, and the number of cells in ganglion cell layer, whereas LPS significantly prevented these alterations. Light exposure increased the mitochondrial bax/cytosolic bax ratio and TBARS levels, whereas LPS prevented these changes. The injection of WT (but not of AG or 5HD) completely blocked the functional and histological protection induced by LPS. These results suggest that LPS provides functional and histological protection against the deleterious effects of constant light through a PI3K-dependent pathway.