2007Basic & Clinical MedicineRequires access

Animal model of cognitive impairment induced by cerebral ischemia reperfusion in diabetic rats

Jin Zhi-gao

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Abstract

Objective To prepare a novo model of cognitive impairment induced by cerebral ischemia reperfusion in diabetic rats. Methods Seventy female Wistar rats were randomly divided into 4 groups: normal control group, ischemic group, diabetic sham-operation group and diabetic ischemic group. Streptozotocin was injected i.p. at a dose of 60 mg/kg, 3 days before the preparation of experimental ischemia. The method used to produce cerebral ischemia was the two-vessel occlusion followed by re-perfusion. After 1-month recovery the animal model with cognitive impairment was confirmed by behavioral assessment. Learning and memorial behaviors of the rats were investigated by a passive and active avoidance response tests and a spatial version of the Morris water maze test. Neuron loss in the area of hippocampus was determined by the pathological H-E staining method. Results The performance of passive avoidance in diabetic cerebral ischemia reperfusion was significantly impaired. The step-down latency of the passive avoidance response of the model rats was shorter, especially at 5th min after training (P0.01). In active avoidance training, the training times of the model group were significantly more than that of the other three groups (P0.001). The swimming time of the rats in Morris water maze in model group was significantly shorter than that in other groups (P0.01). The swimming distance of rats in model group was the shortest amongall 4 groups(P0.05). Conclusion The cognitive ability in diabetic rats with cerebral ischemia 30 days after being induced was significantly declined as compared with the other three groups and diabetes can promote neuronal damage of the brain via cerebral ischemia.

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Objective To prepare a novo model of cognitive impairment induced by cerebral ischemia reperfusion in diabetic rats. Methods Seventy female Wistar rats were randomly divided into 4 groups: normal control group, ischemic group, diabetic sham-operation group and diabetic ischemic group. Streptozotocin was injected i.p. at a dose of 60 mg/kg, 3 days before the preparation of experimental ischemia. The method used to produce cerebral ischemia was the two-vessel occlusion followed by re-perfusion. After 1-month recovery the animal model with cognitive impairment was confirmed by behavioral assessment. Learning and memorial behaviors of the rats were investigated by a passive and active avoidance response tests and a spatial version of the Morris water maze test. Neuron loss in the area of hippocampus was determined by the pathological H-E staining method. Results The performance of passive avoidance in diabetic cerebral ischemia reperfusion was significantly impaired. The step-down latency of the passive avoidance response of the model rats was shorter, especially at 5th min after training (P0.01). In active avoidance training, the training times of the model group were significantly more than that of the other three groups (P0.001). The swimming time of the rats in Morris water maze in model group was significantly shorter than that in other groups (P0.01). The swimming distance of rats in model group was the shortest amongall 4 groups(P0.05). Conclusion The cognitive ability in diabetic rats with cerebral ischemia 30 days after being induced was significantly declined as compared with the other three groups and diabetes can promote neuronal damage of the brain via cerebral ischemia.

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Available abstract

Objective To prepare a novo model of cognitive impairment induced by cerebral ischemia reperfusion in diabetic rats. Methods Seventy female Wistar rats were randomly divided into 4 groups: normal control group, ischemic group, diabetic sham-operation group and diabetic ischemic group. Streptozotocin was injected i.p. at a dose of 60 mg/kg, 3 days before the preparation of experimental ischemia. The method used to produce cerebral ischemia was the two-vessel occlusion followed by re-perfusion. After 1-month recovery the animal model with cognitive impairment was confirmed by behavioral assessment. Learning and memorial behaviors of the rats were investigated by a passive and active avoidance response tests and a spatial version of the Morris water maze test. Neuron loss in the area of hippocampus was determined by the pathological H-E staining method. Results The performance of passive avoidance in diabetic cerebral ischemia reperfusion was significantly impaired. The step-down latency of the passive avoidance response of the model rats was shorter, especially at 5th min after training (P0.01). In active avoidance training, the training times of the model group were significantly more than that of the other three groups (P0.001). The swimming time of the rats in Morris water maze in model group was significantly shorter than that in other groups (P0.01). The swimming distance of rats in model group was the shortest amongall 4 groups(P0.05). Conclusion The cognitive ability in diabetic rats with cerebral ischemia 30 days after being induced was significantly declined as compared with the other three groups and diabetes can promote neuronal damage of the brain via cerebral ischemia.

Key concepts: Morris water navigation task, Medicine, Ischemia, Streptozotocin, Hippocampus, Water maze, Anesthesia, Animal model

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