摘要
目的探讨新生大鼠脑室周围白质软化(PVL)模型侧脑室室管膜下区和脉络丛酪氨酸蛋白激酶(JAKs)-信号转导和转录激活因子(STATs)信号转导途径的变化。方法采用右侧颈总动脉结扎并4h6%氧气处理,建立2日龄SD大鼠缺氧缺血(HI)PVL模型,对照组进行假手术,不进行缺氧处理。HI后0h、3h、6h、12h、1d、3d、7d处死动物,用免疫组化方法检测室管膜下区和脉络丛P-JAK2、P-STAT3表达的变化。结果与对照组相比,实验组大鼠P-JAK2、P-STAT3明显升高,P-JAK2、P-STAT3在HI后即刻就有表达,1d达峰,7d仍高于对照组水平,差异有统计学意义(P<0.01)。结论HI后侧脑室室管膜下区和脉络丛JAKs-STATs途径被激活,该途径可能参与PVL的病理生理过程。
Objective To examine the changes of JAKs-STATs pathway in the subventrieular zone and choroid plexus of neonatal rats with PVL. Methods A PVL model was established by right common carotid artery ligation followed by 4 h 6% oxygen exposure in 2-day-rat, the neonatal rats performed a sham operation, without hypoxia-ischemia were used as the control group. The rats were sacrificed at 0 h, 3 h, 6 h, 12 h, 1 d, 3 d, 7 d of HI, and the brain tissues were collected, immunohistochemistry was applied to detect the expression of P-JAK2 and P-STAT3. Results The expression levels of P-JAK2 and P-STAT3 increased significantly after HI, peaked at 1 d, and remained at a higher level than control until 7 days of HI, the difference was significant (P〈 0. 01). Conclusion HI resulted in the activation of JAKs-STATs pathway in the subventricular zone and choroid plexus, and this pathway might participated in the pathophysiological process of PVL.
出处
《四川大学学报(医学版)》
CAS
CSCD
北大核心
2008年第5期744-747,共4页
Journal of Sichuan University(Medical Sciences)