Oroxylum indicum ameliorates D-galactose-induced aging related memory impairments via enhancing rat hippocampal neurogenesis

Brain aging significantly affects human lives, particularly among the elderly, leading to various diseases and constituting memory and cognitive decline. Hippocampal neurogenesis, the process of generating new neurons throughout life, decline with aging, which contribute to cognitive decline and dementia. D-galactose (D-gal) induces brain aging by increasing oxidative stress and inflammation, resulting in neurodegeneration and memory dysfunction. Oroxylum indicum fruit extract (OIFE), a traditional Thai herb, possesses strong antioxidant and neuroprotective properties. We investigated whether OIFE extract mitigates D-gal-induced memory decline, assessing its phytochemical profile, antioxidant capacity and neuroprotective effects. The results revealed that OIFE possessed strong phytochemical properties using measures such as total phenolic content (TPC), total flavonoid content (TFC), 2,2-diphenyl-1-picrylhydrazyl (DPPH), ferric reducing antioxidant power (FRAP), and high-performance liquid chromatography-ultraviolet (HPLC-UV). Liver and kidney function tests on blood samples showed no significant differences among the groups. For memory function testing, sixty male Sprague Dawley rats were divided into six groups and treated with OIFE (125 or 250 mg/kg, p.o.) and D-gal (50 mg/kg, i.p.) for eight weeks. D-gal administration resulted in significant memory deficits (accessed via the novel object location [NOL] and novel object recognition [NOR] test). These deficits were correlated with a decrease in the number of immature neurons and reduced neuronal cell survival in the subgranular zone (SGZ), as observed using doublecortin (DCX) and 5-Bromo-2'-deoxyuridine/Neuronal nuclear protein (BrdU/NeuN) immunofluorescence staining, respectively. However, co-treatment with OIFE ameliorates D-gal-induced these impairments. Therefore, OIFE could mitigate memory and neurogenesis impairments in D-gal-induced brain aging in rats.