脑出血后的炎症机制  

Mechanisms of Inflammation after Intracerebral Hemorrhage

作　　者：刘娜娜[1] 祝继原[1] 戚基萍[1] 吴鹤[1] 

机构地区：[1]哈尔滨医科大学附属第一医院病理科,哈尔滨150001

出　　处：《医学综述》2015年第10期1732-1735,共4页Medical Recapitulate

基　　金：国家自然科学基金青年科学基金(81200885)

摘　　要：炎症可以加重脑出血后的继发性损伤,并在其中发挥重要作用。脑出血后,血肿成分通过激活小胶质细胞触发炎性通路。活化的小胶质细胞释放促炎性细胞因子和炎症趋化因子来募集周围的炎性细胞。渗入的炎性细胞和小胶质细胞释放炎性因子,最终导致细胞死亡。死亡的细胞释放危险相关分子,加重炎症反应,最终导致脑水肿和神经功能障碍。该文对脑出血后的炎症机制及其最新研究进展予以综述,以期发现脑出血新的治疗靶点。Numerous studies have demonstrated that inflammation can aggravate the secondary injury after intracerebral hemorrhage,which is very important.Hematoma components activate inflammatory via acti-vating microglia after intracerebral hemorrhage.Activated microglia release inflammatory cytokines and che-mokines which recruit inflammatory cells.The recruited inflammatory cells and microglia induce cell death via releasing inflammatory cytokines.Danger-associated molecules released from dead cells aggravates inflam-matory injury,which lead to cerebral edema and neurological deficit ultimately.To identify new therapeutic targets for the treatment of intracerebral hernorrhag,here summarizes recent progress concerning the mecha-nism of intracerebral hernorrhag-induced inflammation.

关 键 词：脑出血 炎症 小胶质细胞 TOLL样受体4 

分 类 号：R363.21[医药卫生—病理学]