Abstract
Abstract: :
Purpose: ApoE–/– deficient mouse (apoE–/–), experimental model of hypercholesterolemia, developes atherosclerosis and shows morphological and ultrastructural retinal alterations. We studied angiogenic–related molecules in this animal model, and the effect of diet supplementation with a multivitamin complex (MC, Nutrof®) lutein and glutathione. Methods: Three months old mice were caged in groups (n=5): control (wild type, wt), apoE–/– (AE) and 2 groups treated with multivitamin complex (15 mg/kg/day, MC15; 50 mg/kg/day, MC50). Total cholesterol, triglycerides and lipid peroxidation (TBARS) were measured in plasma. TBARS, VEGF expression (western blot) and MMP–2 activity (zymography) were determined in eyecups homogenates. Ultrastructure was analyzed by electron microscopy. Results: ApoE–/– mice, with an increased total cholesterol (P<0.05) and triglycerides (P<0.05), exhibit a sistemic and retinal lipid peroxidation increase (P<0.05, P<0.01, respectively) in comparison to wild type. Moreover, this animal model shows an augmented ocular VEGF expression and gelatinase activity (P=0.056, P<0.05, respectively). In addition, AE presents retinal alterations as basal laminar deposits and degradation of retinal pigment epithelium and Bruch's membrane. MC50 group shows retinal lipid peroxidation, VEGF expression and MMP–2 activity reduction compared to AE (P<0.05, P=0.057, P<0.05, respectively). However, MC15 mice did not show significant reduction compared to AE group. In contrast to MC15 group, MC50 treatment prevented ultrastructural changes in this animal model. Conclusions: MC treatment could prevent retinal alterations in apoE–/– mice, at least by reducing VEGF expression and MMP–2 activity. These results suggest that antioxidant treatments could help preventing Bruch's membrane degradation and posterior angiogenic processes.
Keywords: antioxidants • Bruch's membrane • retinal degenerations: cell biology