Aging is a natural progressive decline in the biological function of cells. Age-related changes in the cornea can affect its ability to refract light or repair itself. Platelet-rich plasma (PRP) has a promising role in regenerative medicine and evidenced its efficacy in multiple fields, but in corneal aging has not yet been elucidated. The present work was performed to estimate the regenerative antioxidant effect of PRP on corneal aging in rats. Rats were assigned into two main groups: (GI) adult group and (GII) aged group. The adult group was divided into GIa (adult rats), GIb (adult-saline treated), and GIc (adult-PRP treated). The aged group was divided into GIIa (aged rats) and GIIb (aged, PRP treated). PRP was administered by a single subconjunctival injection. After 10 days, histological, ultrastructural, immunohistochemical, and morphometrical investigations were carried out. Examination of the corneal sections of the aged group revealed corneal epithelial thinning, shedding of the surface epithelium with loss of desmosomal junction, and irregularity in Bowman’s membrane. Disorganized widely spaced collagen bundles and neovascularization were detected in corneal stroma associated with thickening in Descemet’s membrane. Ultrastructural examination revealed shrunken hyperchromatic nuclei, swollen mitochondria, and scanty cytoplasm with a strong nuclear reaction for caspase-3 immunostaining. Moreover, antioxidant/free radicals’ imbalance was detected by the increase of malondialdehyde (MDA) level with a decrease of glutathione peroxidase (GPx) and superoxide dismutase (SOD) levels. In contrast, GIIb (aged, PRP treated) section examination revealed a restoration of the thickness of the corneal epithelial layer and Descemet’s membrane with an amendment of collagen fiber regularity that is associated with weak nuclear reaction to caspase-3 and recovery of the balance in the redox state. These findings proved the effectiveness of PRP as a promising regenerative treatment for the age-associated changes in the cornea.