The Effect of Combined Therapy of Exercise and Nootropic Agent on Cognitive Function in Focal Cerebral Infarction Rat Model
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Objective To investigate the eff ect of combined therapy of exercise and nootropic agent on cognitive function in a focal cerebral infarction rat model. Method Forty 10-week old male Sprague-Dawley rats were subjected to photothrombotic cerebral infarction of the left parietal lobe. All rats were randomly divided into 4 groups: group A was photothrombotic cerebral infarction rats without any treatment (n=10); group B was photothrombotic cerebral infarction rats with swimming exercise (n=10); group C was photothrombotic cerebral infarction rats with oral administration of acetyl-L-carnitine (n=10);group D was photothrombotic cerebral infarction rats with swimming exercise and oral administration of acetyl-L-carnitine (n=10). Cognitive function was evaluated using the Morris water maze test on the 1st day, and the 1st,2nd, and 4th week after the induction of cerebral infarction. Th e activity of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) in the hippocampus were measured. The neuronal cells of the hippocampus were histopathologically evaluated. Results Th e escape latency was shorter in groups B, C, and D than in group A. However, the diff erences were not statistically signifi cant at the 1st, 2nd and 4th week. Th e activity of SOD was the highest in group D. Th e level of MDA was the lowest in group D. We observed more normal neuronal cells in groups B, C, and D. Conclusion Th e combined therapy of exercise and nootropic agent was helpful in ameliorating oxidative stress in the focal cerebral infarction rat model. However, the effect did not translate into improvement of cognitive function.
Abstract
Objective To investigate the eff ect of combined therapy of exercise and nootropic agent on cognitive function in a focal cerebral infarction rat model. Method Forty 10-week old male Sprague-Dawley rats were subjected to photothrombotic cerebral infarction of the left parietal lobe. All rats were randomly divided into 4 groups: group A was photothrombotic cerebral infarction rats without any treatment (n=10); group B was photothrombotic cerebral infarction rats with swimming exercise (n=10); group C was photothrombotic cerebral infarction rats with oral administration of acetyl-L-carnitine (n=10);group D was photothrombotic cerebral infarction rats with swimming exercise and oral administration of acetyl-L-carnitine (n=10). Cognitive function was evaluated using the Morris water maze test on the 1st day, and the 1st,2nd, and 4th week after the induction of cerebral infarction. Th e activity of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) in the hippocampus were measured. The neuronal cells of the hippocampus were histopathologically evaluated. Results Th e escape latency was shorter in groups B, C, and D than in group A. However, the diff erences were not statistically signifi cant at the 1st, 2nd and 4th week. Th e activity of SOD was the highest in group D. Th e level of MDA was the lowest in group D. We observed more normal neuronal cells in groups B, C, and D. Conclusion Th e combined therapy of exercise and nootropic agent was helpful in ameliorating oxidative stress in the focal cerebral infarction rat model. However, the effect did not translate into improvement of cognitive function.
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