Abstract:

Objective To explore the role of microRNA-181b (miR-181b) in cerebral ischemic injury in vivoand its mechanism. Methods Using middle cerebral artery occlusion (MCAO) model to mimic ischemic injury in vivo, the heat shock protein A5(HSPA5)protein level was determined by using Western blotting. The extent of neural cell loss in ischemic cortex after MCAO was assessed by Nissl staining. Neurological score was performed to evaluate the degree of cerebral ischemic injury after MCAO. Results We found that miR-181b antagomir down-regulated miR-181b expression levels in cerebral ischemic cortex of mice after MCAO(P<0.05,n=3). MiR-181b antagomir improved neurological deficit of mice at 24 hours after transient MCAO (P<0.05,n=6). HSPA5 protein levels were significantly up-regulated in ischemic cortex of mice after MCAO，and miR-181b antagomir further up-regulated HSPA5(P<0.05,n=3).Consequently, miR-181b antagonists attenuated neural cell loss in ischemic cortex after MCAO(P<0.05,n=3). Conclusion MiR-181b plays an important role in ischemic injury of mice through regulating HSPA5 protein level.

Key words: Middle cerebral artery occlusion, MicroRNA-181b, Heat shock protein A5, Western blotting, Nissl staining, Behavioral detection, Mouse