动物造模,脑缺血 z-bio 2022-08-09 437

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

　　Methods According to the random number table method, 40 SPF SD male rats were randomly divided into sham operation group, model group, experimental group and control group. For the animal model of middle cerebral artery occlusion (MCAO), the rats in the sham operation group were only threaded without ligation; the rats in the experimental group were given regular aerobic exercise (treadmill running) every day: the exercise intensity was 20 m/min, 3 times a day, 20 min each time, with 2 h interval between each time. The rats in the control group were given 1.08 mg/mL nimodipine by gavage every day. Laser speckle imaging to observe the changes of blood flow in rat cerebral cortex; EEG to detect the changes of total power in rat cerebral cortex; 2,3,5-triphenyltetrazolium chloride (2,3,5-triphenyltetrazolium chloride, Brain-derived neurotrophic factor (BDNF), growth-associated protein 43 (GAP43) and brain-derived neurotrophic factor (BDNF), growth-associated protein 43 (GAP43) in the brain tissue of rats in each group were detected by western blotting expression.

　　Results Compared with the sham operation group, the cerebral cortical blood perfusion, the total power of the cerebral cortex, the expressions of BDNF and GAP43 in the model group, the experimental group and the control group were significantly decreased (P < 0.05), and the infarct size was significantly increased. (P < 0. 05), compared with the model group, the cerebral cortical blood perfusion, the total power of the cerebral cortex, the expressions of BDNF and GAP43 in the experimental group and the control group were significantly increased (P < 0. 05), and the infarction was significantly higher than that in the model group. The area decreased significantly (P < 0.05).

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