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An Innovative Running Wheel-based Mechanism for Improved Rat Training Performance
Published on: September 19, 2016
Repeated short-term daily exercise ameliorates oxidative cerebral damage and the resultant motor dysfunction after
Michiru Hamakawa1, Akimasa Ishida, Keigo Tamakoshi
1Department of Physical Therapy, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-minami, Higashi-ku, Nagoya, Aichi 461-8673, Japan ; Okinawa Rehabilitation Center Hospital, 2-15-1 Hiyagon, Okinawa, Okinawa 904-2173, Japan.
Abstract:
Long-term exercise prior to brain ischemia enhances the activities of antioxidant enzymes and leads to a significant reduction in brain damage and neurological deficits in rats subjected to transient middle cerebral artery occlusion. However, it has not been established whether relatively short-term exercise generates similar results following middle cerebral artery occlusion. We aimed to determine whether short-term exercise could reduce oxidative damage and prevent sensori-motor dysfunction. Male Wistar rats were subjected to perform daily exercise on a treadmill for 30 min at a speed of 15 m/min for 3 weeks, followed by a 90-min middle cerebral artery occlusion. Animals were assessed after middle cerebral artery occlusion for neurological deficits and sensori-motor function. Brain tissues were processed to evaluate infarct volume and oxidative damage. Oxidative stress was assessed using immunohistochemistry for 4-hydroxy-2-nonenal-modified proteins and 8-hydroxy-2'-deoxyguanosine. Antioxidant enzymes were evaluated using immunohistochemistry for thioredoxin and activity assay for superoxide dismutase. Exercise for 3 weeks decreased the severity of paralysis and impairment in forelimb motor coordination. Furthermore, exercise had effect on superoxide dismutase and reduced the infarct volume and the number of cells immunopositive for 4-hydroxy-2-nonenal-modified proteins and 8-hydroxy-2'-deoxyguanosine. Our results suggest that pre-conditioning treadmill exercise for 3 weeks is useful for ameliorating ischemia-induced brain injury.
