The mechanisms of JAK2/STAT3 signal pathway in ischemic brain injury in rats

Objective To observe the expression of P-JAK2 and P-STAT3 protein after focal cerebral ischemic and reperfusion injury in rats and to study the effects of JAK2/STAT3 signal pathway in ischemia brain injury.Methods Middle cerebral artery occlusion/reperfusion rat's models were performed by using modified filament method.Western blot analysis was used to detect the expression of P-JAK2 and P-STAT3 protein.TUNEL was used to examine the apoptosis cells.Furthermore,the effects of inhibiting JAK2 phosphorylation,with AG490 (a JAK2 phosphorylation inhibitor) on post-ischemic neuronal damage was evaluated.Results Western blotting analysis showed very little P-JAK2 and P-STAT3 protein in the pere-ischemic region after 3h reperfusion following transient MCAO in rats,started to increase rapidly at 12h reperfusion,peaked at 24h reperfusion and thereafter decreased slightly.The apoptosis cells also increased obviously after cerebral ischemic and reperfusion injury in rats and peaked at 24~48h reperfusion.AG490 prevented the post-ischemic JAK2 and STAT3 phosphorylation and significantly decreased the number of apoptotic cells.Conclusion The studies show focal ischemia-reperfusion induced JAK2 and STAT3 phosphorylation.JAK2/STAT3 signal pathway playes a role in the pathophysiological process of cerebral ischemia/reperfusion cell injury and renovation.