Antioxidant and neuro-modulatory effects of niacin prevent D-galactose-induced behavioral deficits and memory impairment.

Abstract

Aging is an invincible phenomenon that is a risk factor for the development of neurological disorders such as anxiety, depression, and memory decline that are prominent in aging. The present study aims to evaluate the effect of Niacin (Nn) on D-galactose (D-Gal)-induced behavioral deficits and memory impairment in rats. In the experiment, forty-eight male albino Sprague dwaley rats were divided on a random basis into six groups (n = 8): Veh + Veh, Veh + Nn (low dose), Veh + Nn (high dose), Veh + D-Gal, D-Gal+Nn (low dose), D-Gal+Nn (high dose). 300 mg/kg/mL drug doses of D-Gal, while low doses (25 mg/kg/mL) and high doses (50 mg/kg/mL) of Nn were used in this study. Animals received their respective treatment for 14 days (intraperitoneally, once daily). After 14 days, animals were subjected to different behavioral tests including light-dark box activity, elevated plus maze test (for anxiety), and tail suspension test (for depression). A Morris water maze test was performed to evaluate short-term and long-term memory performance. After behavioral tests, decapitation was performed and brains were collected and stored for biochemical and neurochemical analysis. Behavioral analysis revealed that Nn alleviated the anxiety and depression-like symptoms and memory decline induced by D-Gal. D-Gal-induced decreased antioxidant enzymes, and acetylcholine levels, while increased oxidative stress markers, neuro-inflammatory cytokines, serotonin metabolism, and acetylcholinesterase (AChE) activity were prevented by Nn administration at both doses. In-silico studies showed that Nn has a potential to inhibit AChE activity with a binding affinity of -5.0 kcal/mol. In conclusion, Nn as an antioxidant and neuromodulator could be helpful for treating aging and associated psychiatric illnesses.