Abstract
Diabetic retinopathy (DR) is a major microvascular complication that can lead to severe visual impairment in patients with diabetes. The elevated oxidative stress and increased reactive oxygen species (ROS) production induced by hyperglycemia have been reported to play an important role in the complex pathogenesis of DR. Astaxanthin (AST), a natural carotenoid derivative, has been recently recognized as a strong free radical scavenger and might, therefore, be beneficial in different diseases, including DR. In this study, we evaluated the potential role of AST as an antioxidative and antiapoptotic agent in protecting retinal cells and also investigated the involvement of the PI3K/Akt/Nrf2 pathway in AST-mediated effects. We treated high glucose-cultured mouse photoreceptor cells (661W) with different concentrations of AST and analyzed ROS production and cell apoptosis in the different regimens. Moreover, we also analyzed the expression of PI3K, Akt, Nrf2, and Phase II enzymes after AST treatment. Our results showed that AST dose-dependently reduced ROS production and attenuated 661W cell apoptosis in a high glucose environment. Importantly, its protective effect was abolished by treatment with PI3K or Nrf2 inhibitors, indicating the involvement of the PI3K/Akt/Nrf2 pathway. These results suggest AST as a nutritional supplement that could benefit patients with DR.
Highlights
Diabetes is a major metabolic disease that can affect different organs through microvascular and macrovascular damages [1]
Our results showed that AST reduced high glucose-induced oxidative stress and attenuated apoptosis of photoreceptor cells by induction of antioxidant enzymes via the PI3K/Akt/Nrf2 pathway
Results indicate that AST activates the PI3K/Akt/Nrf2 pathway, which further contributes to decreasing. These results indicate that AST activates the PI3K/Akt/Nrf2 pathway, which further contributes to the reactive oxygen species (ROS) generated in a high glucose environment
Summary
Diabetes is a major metabolic disease that can affect different organs through microvascular and macrovascular damages [1]. Diabetic retinopathy (DR), a leading microvascular complication of diabetes, is characterized by a progressive increase in vascular permeability, retinal ischemia and edema, and neovascularization, which can result in visual impairment and even legal blindness [2]. Despite the improved understanding of its pathogenesis and the advances in available treatments, the long-term outcome of DR remains poor owing to its complex pathogenesis [3,4]. The continuous search for new modalities to prevent and treat this debilitating complication is essential. Hyperglycemia induces oxidative stress and generates reactive oxygen species (ROS) within the retina [5,6]; the activity of cellular antioxidant enzymes responding to ROS is insufficient to prevent the consequent damages.
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