Aronia melanocarpa anthocyanins attenuate light-induced retinal damage via enhancing photoreceptor cell function and anti-inflammatory effects.

Abstract

Prolonged exposure to excessive light causes retinal photodamage, leading to structural and functional impairment of the retina through pathogenic mechanisms involving oxidative stress, inflammatory responses, and disruption of cellular homeostasis. Aronia melanocarpa anthocyanins (AMA) have shown protective effects against retina degeneration. However, the extremely protective effect of AMA on light-induced retinal damage (LD) and the underlying mechanisms remain unclear. A model of LD was established by exposing Sprague-Dawley rats to intense illumination. This study aims to investigate the prophylactic potential of AMA in mitigating LD. AMA intervention mitigated the attenuation of electroretinogram (ERG) a- and b-wave amplitudes, lessened the atrophy of the outer nuclear layer, and decreased cell loss in the ganglion cell layer. Additionally, increased expression of rhodopsin (RHO) and rod-arrestin (SAG) were observed in the retinas of LD rats following AMA intervention, accompanied by a concomitant downregulation of the pro-inflammatory cytokine tumor necrosis factor α (TNF-α). AMA confers protection against LD through its potential interaction with the Nrf2/Sirt3/SOD2 signaling pathway. In addition to its potent anti-inflammatory and antioxidative stress properties and its ability to promote RHO and SAG regeneration, AMA significantly reduced photoreceptor cell apoptosis in light-damaged retinas. The principal functional component of AMA is cyanidin-3-O-arabinoside, which exhibits the strong binding interactions with RHO and SAG, suggesting a potential role in photoprotection. Our study demonstrates that AMA provides a protective effect on visual function against LD, establishing a foundation for dietary supplements and nutritional interventions for retinal disorders.