الفهرس 
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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
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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.