earticle

영어

Postnatal rat offspring born from prenatal alcohol-intoxiciated pups during pregnancy leads to apoptosis or inhibitation of neurigenesis, which eventually causes neurological impairments. In the present study, the effects of endurance exercise on the level of apoptosis and cell proliferation in the hippocampal dentate gyrus following fetal alcohol syndrome in Sprague-Dawley rats were investigated. Adult female Sprague– Dawley rats weighing 220±10 g were used in the experiment. Total 60 female rats were mated in pairs with adult 30 male Sprague–Dawley rats weighing 300±10g for 48h. After mating, the female rats were housed individually in a plastic home cage. After confirmation of pregnancy, the pups borned from female rats were randomly divided into four groups: the control group, fetal alcohol-treated group, fetal alcohol-treated and moderate-intensity exercise group, and fetal alcohol-treated and swimming exercise group(n=20, respectively). The exercise groups were made to run on a treadmill running and swimming for 60 min per day for 14 consecutive days. Apoptotic cell death in the hippocampal dentrate gyrus was measured by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL) and caspase-3 staining, and cell neurogenesis was detected by 5-bromo-2'-deoxyuridine(BrdU) immunohistochemistry. It was shown that apoptosis and cell proliferation in the hippocampal dentate gyrus were significantly increased following prenatal alcohol injection in Sprague–Dawley rats and that treadmill exercise and swimming suppressed the alcohol-induced increase of apoptosis and cell neurogenesis in the dentate gyrus. The present results suggest that treadmill exercise and swimming may protect neurons from apoptotic death and aids in recovery from the central nervous system sequelae following fetal alcohol syndrome.