脑出血后继发性神经炎症反应特点及其相关信号通路的研究进展

Research Progress on the Characteristics and Relevant Signaling Pathways in Secondary Neuroinflammation after Cerebral Haemorrhage

脑出血会产生局部性的机械性损伤和压迫性损伤,导致脑组织中神经组织的缺血、缺氧、水肿等,最终引发神经炎症反应,导致严重的神经功能障碍。脑出血后继发性神经炎症反应具有急性炎症反应、炎症递质释放、血脑屏障破坏、神经元凋亡和慢性炎症等特点,这些特点与多种信号通路的激活和参与相关,包括核因子κB(NFκB)、Janus激酶/信号转导和转录激活子(JAK/STAT)、丝裂原活化蛋白激酶(MAPK)、磷脂酰肌醇3-激酶/蛋白激酶B(PI3K/Akt)、Toll样受体(TLR)等信号通路。本文综述了脑出血后继发性神经炎症反应的特点及其相关信号通路的作用机制,有助于寻找脑出血后继发性神经炎症反应新的治疗靶点。

Cerebral hemorrhage produces localized mechanical injury and compressive damage,leading to ischaemia,hypoxia and oedema of neural tissues of the brain tissue,which ultimately triggers a neuroinflammation and leads to severe neurological dysfunction.Secondary neuroinflammation afteRcerebral hemorrhage is characterized by acute inflammatory response,inflammatory transmitteRrelease,blood-brain barrieRdisruption,neuronal apoptosis,and chronic inflammation.These characteristics are associated with the activation and involvement of multiple signaling pathways,including nucleaRfactor-kappa B(NF-κB),Janus kinase/signal transduceRand activatoRof transcription(JAK/STAT),mitogen-activated protein kinase(MAPK),phosphoinositide 3-kinase/protein kinase B(PI3K/Akt),and Toll-like receptors(TLR)signaling pathways.This papeRdescribes the characteristics and relevant signaling pathways in secondary neuroinflammation afteRcerebral haemorrhage,which will help to find new therapeutic targets foRsecondary neuroinflammation afteRcerebral hemorrhage.