JAK2－STAT3信号通路在大鼠脑出血模型中的作用

摘要

目的：探讨大鼠脑出血后JAK2－STAT3信号通路的作用机制及与脑水肿的关系。方法健康雄性SD大鼠108只，经尾动脉取血缓慢注射到尾状核区制作大鼠脑出血模型。根据出血时间不同，采用随机数字表法将其分为3h、9h、1d、3d、5d和7d6组，每个组又分为3个亚组：模型组、假手术组和AG490组。采用免疫组织化学和Western印迹检测JAK2、p－JAK2、STAT3和p－STAT3的表达，并测定脑组织含水量。结果与假手术组和AG490组相比，模型组中p－JAK2和p－STAT3大量表达，并于24 h时达到高峰；与模型组相比，AG490组大鼠脑组织含水量在各时间点均较低。结论脑出血后能够激活JAK2－STAT3信号通路，并导致脑组织水肿。%Objective To investigate the role and mechanisms of JAK 2-STAT3 signaling pathway preliminarily in intracerebral hem-orrhageratmodelandtherelationshipbetweenbrainedema.Methods 108healthymaleSDratswereusedtoinduceintracerebralhemor-rhage models .According to the difference of bleeding time ,all rats were randomly divided into six groups .Every group was further divided into three subgroups:model(M),sham(S) and AG490(AG)groups.Both immunohistochemistry and Western blot analysis were used to detect the expressions of JAK2,p-JAK2,STAT3 and p-STAT3.Results Compared with those of sham and AG groups ,the protein levels of p-JAK2 and p-STAT3 were significantly increased in M group and peaked at 24 h.Compared with that of model group ,the water content of rat brain tissues in AG group were lower than that in M group at every time point .Conclusions The JAK2-STAT3 signaling pathway could be activated in in-tracerebral hemorrhage rat model and contributes to brain edema .