摘要
缺血缺氧脑病(Hypoxic-ischemic encephalopathy,HIE)是导致新生儿死亡和婴幼儿神经发育障碍的主要原因,部分患儿有不同程度的神经系统后遗症,如脑瘫、认知和运动功能发育障碍。缺血缺氧可激活JAK2/STAT3信号通路,进而导致小胶质细胞异常活化,引发神经炎症反应;通过下调JAK2/STAT3信号通路可抑制小胶质细胞异常活化,改善神经系统炎性损伤。当前缺血缺氧脑病的治疗方法有限,因此研究小胶质细胞活化的调控机制对于缺血缺氧脑病的治疗具有重要临床价值。本文对JAK2/STAT3信号通路在小胶质细胞活化中的作用及二者相互关系的研究进展作一综述,以期为缺血缺氧脑病的治疗提供新的研究思路。
Hypoxic-ischemic encephalopathy(HIE)is the leading cause of neonatal death and neurodevelopmental disorders in infants.Part of patients have different degrees of neurological sequelae,such as cerebral palsy,cognitive and motor function development disorders.Hypoxia-ischemia may activate JAK2/STAT3 signaling pathway,which leads to the microglia activation and neuroinflammation.Down-Regulating JAK2/STAT3 signaling pathway can inhibit microglia activation and regulate the inflammatory injury of nervous system.At present,the treatment of hypoxic-ischemic encephalopathy is limited,so the study of regulatory mechanism about microglia activation has important value for the treatment of hypoxic-ischemic encephalopathy.This paper summarizes the role of JAK2/STAT3 signaling pathway in microglia activation and analyzes the relationship between them,in order to provide new ideas and strategies for treatment on hypoxic-ischemic encephalopathy.
作者
曾杰
赵亚林
邓博文
李筱叶
徐杰
汪乐
穆晓红
ZENG Jie;ZHAO Ya-lin;DENG Bo-wen;LI Xiao-ye;XU Jie;WANG Le;MU Xiao-hong(The Fourth Department of Orthopaedics,the First Affiliated Hospital of Beijing Chinese Medical University,Beijing 100700,Beijing,China)
出处
《中国骨伤》
CAS
CSCD
2020年第2期190-194,共5页
China Journal of Orthopaedics and Traumatology
