Oral Supplementation with Prunus domestica L. Extract Restores Recognition Memory Impairment Caused by D-Galactose in Rats.

Background/Objectives: Aging-related cognitive decline, linked to oxidative stress and impaired hippocampal neurogenesis, is a major contributor to neurodegenerative disorders. In rodents, this condition can be modeled by D-galactose (D-gal) administration, which induces oxidative stress and recognition memory deficits. Prunus domestica L. (PD), rich in phenolic and flavonoid compounds with antioxidant properties, may counteract such impairments. This study evaluated the effects of PD extract on D-gal-induced memory decline by analyzing its phytochemical content, antioxidant activity, and neuroprotective potential. Methods: Phytochemicals were quantified by colorimetric and pH differential methods, and antioxidant capacity was determined using DPPH and FRAP assays. Male Sprague Dawley rats (12 weeks; n = 12/group) were assigned to 8 groups: vehicle, D-gal, PD (75, 100, or 150 mg/kg), and D-gal + PD (same respective doses). D-gal (50 mg/kg, i.p.) and/or PD were administered by oral gavage daily for 8 weeks. Recognition memory was assessed by the novel object recognition (NOR) test. Hippocampal tissues were processed for immunofluorescence staining of the proliferation marker Ki-67 and superoxide dismutase (SOD) activity using the cytochrome C reduction method. Results: PD extract contained abundant phenolics, tannins, flavonoids, and anthocyanins, and exhibited notable antioxidant activity. D-gal impaired recognition memory, reduced hippocampal cell proliferation, and decreased SOD activity. Co-treatment with PD improved memory performance, enhanced hippocampal neurogenesis, and restored antioxidant enzyme activity. Conclusions: PD extract may protect against D-gal-induced age-related cognitive decline through antioxidant effects and support of hippocampal neurogenesis.