D-galactose induced dysfunction in mice hippocampus and the possible antioxidant and neuro-modulatory effects of selenium

Abstract

Aging is an ultimate reality that everyone has to face. D-galactose (D-gal) has been used extensively to develop aging model. Trace elements such as selenium (Sel) have been used as a potential antioxidant for neuro-protection. The present work aims to develop therapeutic agents such as Sel for the treatment of aging-induced neurological ailments such as anxiety, depression, and memory impairment. For this purpose, mice were treated with D-gal at a dose of 300 mg/ml/kg and various doses of Sel (0.175 and 0.35mg/ml/kg) for 28 days. Behavioural tests were monitored after treatment days. After the behavioural assessment mice were decapitated and their brains were collected. Hippocampi were removed from the brain for biochemical and neurochemical analysis. The present findings of behavioural analysis showed that D-gal induced anxiety and depression-like symptoms were inhibited by both doses of Sel. D-gal induced memory alteration was also prevented by repeated doses (0.175 and 0.35mg/ml/kg) of Sel. Biochemical analysis showed that D-gal induced increase of oxidative stress marker and decrease of antioxidant enzymes in the hippocampus was prevented by Sel administration. An increase in the activity of acetylcholinesterase was also diminished by Sel. The neurochemical assessment showed that D-gal induced increased serotonin metabolism and decreased acetylcholine levels in the hippocampus were restored by repeated treatment of Sel. It is concluded that D-gal induced dysfunction in mice hippocampus caused anxiety, depression, memory impairment, oxidative stress that were mitigated by Sel via its antioxidant potential and modulating capability of serotonergic and cholinergic functions.