Abstract:

Objective To study the effect of dexmedetomidine（Dex）on neural function and Janus kinase 2 （JAK2）/signal transducer and activator of transcription 3（STAT3）pathway in rats with intracerebral hemorrhage. Methods Adult male SD rats were randomly divided into different groups. The model of intracerebral hemorrhage was established，Dex，NC or JAK2 lentivirus were given for intervention. The neurological deficit score（NSS）was evaluated；the pathological changes，the apoptosis and inflammation levels were evaluated. Results After modeling， the DSS scores of intracerebral hemorrhage group were lower than those of the sham group，the apoptosis rate and the expression of NF⁃κB，Bax，Cleaved caspase⁃3，p⁃JAK2，p⁃STAT3，the contents of TNF⁃α，IL⁃6 in brain tissue around hematoma were higher than those of sham group（P < 0.05）. After Dex intervention，the DSS scores of Dex group were higher than those of intracerebral hemorrhage group，and the apoptosis rate and the expression of NF⁃κB， Bax，Cleaved caspase⁃3，p⁃JAK2，p⁃STAT3，the contents of TNF⁃α，IL⁃6 in brain tissue around hematoma were lower than those of intracerebral hemorrhage group（P < 0.05）. After intracerebroventricular injection of JAK2 lentivirus and overexpression of p⁃JAK2，p⁃STAT3 before modeling，the DSS scores of JAK2 lentivirus+Dex group were lower than those of the NC lentivirus + Dex group，the apoptosis rate and the expression of NF ⁃ κB，Bax， Cleaved caspase⁃3，p⁃JAK2，p⁃STAT3，the contents of TNF⁃α，IL⁃6 in brain tissue around hematoma were higher than those of the NC lentivirus+Dex group（P < 0.05）. Conclusion Dex could improve the neurological function and pathological changes of brain tissue around hematoma in rats with intracerebral hemorrhage. This improvement was associated with the inhibition of JAK2 / STAT3 pathway mediated inflammatory response and apoptosis.

Key words:

intracerebral hemorrhage, dexmedetomidine, JAK2/STAT3 pathway, inflammatory response, apoptosis