FAN LICHAO, ZHOU LICHUN
Department of Neurology, Jingxi Campus, Beijing Chao-Yang Hospital, Capital Medical University
Objective: To study the expression and mechanism of action of JAK-STAT signal passage transducing proteins JAK2 and STAT3 in a rat cerebral ischemia reperfusion models.
Methods: Wistar rats (100) were divided into a sham-operation group and a model group with 50 rats in either group, to build cerebral ischemia reperfusion models of rats. After the models have been set up successfully, reperfusion injury was induced, and brain tissues were taken at 2 h, 1 day, 3 days, 7 days and 21 days, and subjected to Western blot and immunofluorescence to deter- mine changes in expressions of p-JAK2 and p-STAT3.
Results: There were significant differences in the expressions of p-JAK2 and p-STAT3 between the model group and the pseu- do-operation group within the same periods (p < 0.05). These expressions were highest in the model group at day 1.
Conclusion: These results indicate that the expressions of p-JAK2 and p-STAT3 are highly enhanced after cerebral ischemia reperfusion. Thus, abnormal activation of JAK2-STAT3 signal transduction passage may be one of the mechanisms involved in nerve cell apoptosis after cerebral ischemia and reperfusion injury.
Cerebral ischemia reperfusion, JAK-STAT signal passage, p-JAK2, p-STAT3