Metformin improved memory impairment caused by chronic ethanol consumption during adolescent to adult period of rats: role of oxidative stress and neuroinflammation.

Abstract Objective Adolescence is a crucial time for brain maturation. We investigated the protective effects of metformin (Met) on behavioral changes, oxidative stress, tumor necrosis factor alpha (TNF-α) and nitrite in adulthood induced by ethanol (Eth) consumption during adolescent to adult period of rats. Materials and Methods The adolescence male rats (21 days old) were treated as: 1) Control, 2) Eth (Eth in drinking water (20 %)), 3–5) Eth-Met50, 100 and 150 mg/kg (Eth in drinking water and Met (50, 100, or 150 mg/kg). After 5 weeks treatment, Morris water maze (MMW) and passive avoidance (PA) tests were done. Results The latency in the MWM test was higher and the latency to enter the dark chamber in the PA test was lower in the Eth group than in control. In Eth-Met100 and 150 groups, they were less than the Eth group. Malondialdehyde (MDA) and nitrite concentration in the hippocampus and cortex of the Eth group were higher than the control group. The thiol content and catalase and superoxide dismutase (SOD) activities in hippocampal and cortical tissues of the Eth group reduced compared to the control group. TNF-α was higher in hippocampal tissues of Eth group animals. Met reversed all of these effects. Conclusion Our findings showed that the protective effects of Met against chronic Eth consumption induced learning and memory impairment were accompanied by decreasing of TNF-a, nitrite and oxidative stress in adolescent rats.