动物造模,脑缺血 z-bio 2022-12-12 281

　　Objective To study the protective mechanism of regular aerobic exercise on brain tissue of rats with cerebral ischemia.

　　Methods According to the method of random number table, 40 male SPF SD rats were randomly divided into sham operation group, model group, experimental group and control group. The model of middle cerebral artery occlusion (MCAO) in rats was made by suture method in model group, experimental group and control group. The rats in sham operation group were only threaded without ligation; The rats in the experimental group took regular aerobic exercise (running on the treadmill) every day: the exercise intensity was 20 m/min, three times a day, 20 minutes each time, and the interval between each time was 2 hours. The rats in the control group were given 1.08 mg/mL nimodipine by gavage every day. The changes of cerebral cortex blood flow were observed by laser speckle imaging; EEG was used to detect the changes of total power of cerebral cortex in rats; 2,3,5-triphenyltetrazolium chloride (TTC) staining was used to detect the cerebral infarction area of rats; The expression of brain-derived neurotrophic factor (BDNF) and growth associated protein 43 (GAP43) in brain tissue of rats in each group was detected by Western blot.

　　Results Compared with the sham operation group, the cerebral cortex blood flow perfusion, total power of cerebral cortex, expression of BDNF and GAP43 in the model group, the experimental group and the control group decreased significantly (P<0.05), and the infarct area increased significantly (P<0.05). Compared with the model group, the cerebral cortex blood flow perfusion, total power of cerebral cortex, expression of BDNF and GAP43 in the experimental group and the control group increased significantly (P<0.05), and the infarct area decreased significantly (P<0.05).

　　Conclusion Regular aerobic exercise can significantly improve the blood flow perfusion and cerebral microvascular circulation disorders in rats with cerebral ischemia, reduce the infarct area of their brain tissues, and inhibit the inflammatory cascade amplification, which may be related to the activation of BDNF/GAP43 pathway.