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Abstract The aim of the present work was to study the neuroprotective and antioxidant effects of swimming exercise and/or melatonin on spatial learning and memory impairment induced by D-galactose in rats. This was carried out by investigating the brain oxidative stress markers and hippocampal structural damage induced by D-galactose. Thirty male albino rats were used (age 2 - 3 months, each weighing 160-200g). The rats were divided into the following groups: 1. Control group (C) (n=6 rats). 2. D-galactose treated group (G group) (n=6 rats). 3. Exercised D-galactose treated group (EG group) (n=6 rats). 4. Melatonin and D-galactose treated group (MG group) (n=6 rats). 5. Combined exercised melatonin and D-galactose treated group (CEMG group) (n=6 rats). In each of the previously mentioned groups spatial learning and memory performance were assessed by Banes maze test, the extent of neuronal damage in the hippocampus was evaluated with histological and morphometric assessment and the extent of brain oxidative stress biomarkers including MDA and SOD activity in the brain tissue homogenate were also measured. The results showed that D-galactose caused significant increase in mean number of errors and mean of escape latency per day in day 1 of acquisition phase and day 5 of probe phase of Barnes maze test denoting significant impairment in spatial learning and memory performance when compared to (C) group. It also caused significant increase in MDA and significant decline in SOD activity in brain tissue homogenate denoting brain oxidative stress. The histopathological and morphometric findings showed significant damage in hippocampi of D-galactose treated rats. In (EG) ,(MG) and (CEMG) groups, all treatments caused significant decline in mean number of errors and mean of escape latency per day in day 1 of acquisition phase and day 5 of probe phase of Barnes maze test denoting significant improvement in spatial learning and memory performance when compared to (G) group. All treatments caused significant decline in hippocampal damage or protecting it from damage when compared to (G) group, but the combined and melatonin treatment had better effect on decreasing hippocampal damage in CA3 and DG induced by Dgalactose than swimming exercise did. They also caused significant decline in MDA, exercise and combined treatment caused significant elevation in SOD activity in brain tissue homogenate but level of SOD activity in brain tissue homogenate of (MG) group was insignificantly changed when compared to (G) group. The combined treatment had better effect on elevating the level of SOD activity in brain tissue homogenate than either treatment alone did. It was clear that D-galactose caused significant spatial learning and memory impairment due to oxidative stress that led to hippocampal damage and all treatments had antioxidant effect that combated the oxidative stress Summary - 133 - induced by D-galactose and thereby protected the hippocampus from damage so the spatial learning and memory performance in treated groups was better than (G) group and insignificantly changed when compared to (C) group. |