Neuroprotection Of TSA On Cerebral Ischemia/Reperfusion Injury Via JAK/STAT Signal Pathway

Object:To investigate the effects of trichostatin-A(TSA)on Cerebral ischemia/reperfusion injury, and whether the effects are executed by Janus kinase/signal transducer and activator of transcription (JAK/STAT) signal pathway.Patients and methods:Adult male Sprague-Dawley rats weighing200-250g were randomly divided into3groups:sham-operated group, ischemia/reperfusion group(I/R group), TSA group,12rats per group; In I/R group, rats were prepared following improved transient Middle cerebral artery occlusion(MCAO) in right middle cerebral artery with90-minute ischemia and24-hour reperfusion, sham-operated group was exactly the same with I/R group except putting suture into middle cerebral artery, rats in TSA group were injected with TSA in penile vein20min before the MCAO.After24h reperfusion, the neurological deficit scores were evaluated, and then rats were sacrificed to measure infarct volume by TTC staining and test the protein expression of JAK2、p-JAK2.Results:1.The impacts of TSA on neurological deficits:TSA treatment could significantly improve the neurological deficits compared with the I/R group (p<0.05). 2.The impacts of TSA on cerebral infarct volume:TSA treatment could significantly decrease the infarct volume compared with the I/R group (p<0.05).3.The impacts of TSA on JAK2protein:low level of JAK2expressed in each group, and there were no statistical difference between groups (p>0.05).4.The impacts of TSA on p-JAK2protein:low level of p-JAK2expressed in sham-operated group; the TSA treatment group could significantly decrease the expression of p-JAK2protein compared with the I/R group (p<0.05).Conclusion:TSA can reduce the Cerebral ischemia/reperfusion injury, through the inhibition of JAK/STAT signal pathway mediated by p-JAK2.