Abstract:

 Objective   To study the effects of ischemic preconditioning (IP) on expression of VEGF,GLUT1 and BAI1, and to explore the neuroprotective mechanism of ischemic preconditioning in focal cerebral infarction rats. Methods   Transient middle cerebral artery occlusion (MCAO) was done for 15 min to induce IP, and a permanent MCAO model was established at 48 h after ischemic reperfusion. Nerve function score, brain water content, pathological changes in cerebral tissue, and expressions of VEGF, GLUT1 and BAI1 were studied. Results   IP significantly alleviated neurological and histological injury after PMCAO. Immunohistochemical examination and ELISA revealed higher expression of VEGF and GLUT1 and lower expression of BAI1 in the experimental group than in the control group, with BAI1 negatively correlated with VEGF. Conclusion   IP induced brain ischemic tolerance and provided significant protection to the brain following PMCAO. This protection is probably achieved through IP-triguedmicrocirculation enhancement and energy supply.

Key words: Ischemic preconditioning; Brain ischemic tolerance; Vascular endothelial growth factor; Cerebral infarction