Wang Yan and Wang Chengji
Objective: To observe the effect of exercise training on cognitive functions of a diabetic rat model.
Methods: Male SD rats were given a high fat and high sugar diet, except for the control group. Afte rfour weeks, 35 mg /kg STZ has intraperitoneally injected to establish type 2 diabetes model rats. After successful modelling, rats were randomly divided into the model group, model + exercise group. Animals performed five days of consecutive treadmill exercise (60 min/day) with 22 m/min speeds for 60 days. After 60 days, Morris water maze task was used in the behavior test. Then rats were weighed, and blood samples were obtained to detect blood glucose. Some animals are sacrificed to prepare serum to detect glycosylated hemoglobin. Brain tissues were taken to detect the protein expressions of HMGB1-/RAGE-/NF-κB signal pathway. The brains of other animals were perfused and taken for RAGE and NF-κB immunohistochemical staining.
Results: Compared with the control group, escape latency and probe distance in the model group are significantly prolonged, the swimming time of the target quadrant is obviously shortened, and the number of platform crossing has been significantly reduced. The average grey values of NF-κB and RAGE has been significantly decreased. Expressions of HMGB1, RAGE,p-NF-кBp65 and p-IкBα were significantly up-regulated(P<0.05 or P<0.01). Compared with the model group, escape latency and probe distance are significantly shortened, swimming time in the target quadrant was prolonged and increased the number of crossing platform, it also reduced the fasting blood glucose, increased body weights, reduced the level of glycated hemoglobin, and significantly increased the mean gray values of NF-κB and RAGE. The protein expressions of HMGB1, RAGE, p-NF-кBp65 and p-IкBα are decreased in model + exercise group.
Conclusion: Exercise training can ameliorate the cognitive dysfunction of diabetic rats, its mechanism may be related to lower blood glucose, lower the level of glycated hemoglobin and improvement of the HMGB1 /RAGE/NF-κB pathway in the brain tissue