Can metformin modulate the retinal degenerative changes in a rat model of retinitis pigmentosa?

Abstract

Retinitis pigmentosa (RP) affects over a million people worldwide, characterized by photoreceptor cell death, progressive retinal degeneration, and visual loss. Metformin is demonstrated as a potential therapeutic approach for preventing light-induced retinal degeneration by decreasing apoptosis and oxidative stress. This work aimed to investigate the effect of metformin on the retina of the N-Ethyl-N-nitrosourea (ENU) induced rat model of RP. Eighteen adult male Wistar rats were divided into two groups. Group I: normal vehicle control (N = 6). Group II: ENU-induced photoreceptor degeneration (N = 12) received a single intraperitoneal injection of ENU at a 600 mg/kg dose. Rats in group II were equally divided into two subgroups: IIa: photoreceptor degeneration-induced group and IIb: metformin-treated group (200 mg/kg) for seven days. Specimens from the retina were processed for light and electron microscopy. In ENU treated group, the retina revealed vacuolations and morphological changes in the glia (Müller cells and microglia) and blood capillaries. Increasing caspase-3 (apoptotic marker), iNOS (oxidative stress marker), CD68 (macrophage marker) and glial fibrillary acidic protein (GFAP) expression were detected. In the metformin-treated group, the retinal vacuolations reduced with the morphological improvement in the glia and blood capillaries. Caspase-3, iNOS, CD68, and GFAP expression decreased. Metformin was found to have a neuroprotective effect on the retina in ENU induced rat model of RP