Modulation of hyperglycemia induced oxidative stress-mediated retinal angiogenesis with astaxanthin in vitro and in vivo.

Diabetic retinopathy (DR), a debilitating microvascular complication, is the major cause of
vision loss in the diabetic population. Vascular endothelial growth factor (VEGF) plays a
detrimental role in the pathogenesis of DR. There were compelling pieces of evidence for the
involvement of hypoxia and endoplasmic reticulum stress in the upregulation of VEGF under
diabetic conditions. Thus, targeting VEGF and its associated pathways is an effective strategy
to control DR. Astaxanthin has been reported to possess beneficial effects in the treatment of
several ocular diseases. Hence, we aimed to understand the underlying mechanism of
astaxanthin in protecting the retinal cells in vitro (ARPE-19 cells) and in vivo (streptozotocin�induced diabetic rats). Initially, we found that high glucose/ hypoxia-mediated generation of
ROS and lipid peroxidation in ARPE-19 cells were significantly declined upon astaxanthin
treatment in a dose-dependent manner. Similarly, the nitric oxide, protein carbonyl, and lipid
peroxide levels were significantly increased in diabetic group compared to control and
astaxanthin treated groups.