Naringin alleviates cognitive impairment, mitochondrial dysfunction and oxidative stress induced by D-galactose in mice

Abstract

Role of mitochondrial dysfunction and oxidative stress has been well documented in aging and related disorders such as Alzheimer's disease. Bioflavonoids have been reported to have a therapeutic potential against several age related processes. Bioflavonoids are being used as a neuroprotectants in the treatment of various neurological disorders including aging. Therefore, present study has been conducted in order to explore the possible role of naringin against D-galactose induced cognitive dysfunction, oxidative damage and mitochondrial dysfunction in mice. Chronic administration of D-galactose (100 mg/kg) for 6 weeks significantly impaired cognitive performance (both in Morris water maze and elevated plus maze), locomotor activity, oxidative defense and mitochondrial complex (I, II and III) enzymes activities as compared to sham group. Six weeks naringin (40 and 80 mg/kg) treatment significantly improved cognitive performance, oxidative defense and restored mitochondria complex enzyme activities as compared to control (D-galactose). Naringin treatment significantly attenuated acetylcholine esterase activity in D-galactose treated mice. In conclusion, present study highlights the potential role of naringin against D-galactose induced cognitive impairment, biochemical and mitochondrial dysfunction in mice.