CAJ | 학술논문

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。
염증가이가중뇌출혈후적계발성손상，병재기중발휘중요작용。뇌출혈후，혈종성분통과격활소효질세포촉발염성통로。활화적소효질세포석방촉염성세포인자화염증추화인자래모집주위적염성세포。삼입적염성세포화소효질세포석방염성인자，최종도치세포사망。사망적세포석방위험상관분자，가중염증반응，최종도치뇌수종화신경공능장애。해문대뇌출혈후적염증궤제급기최신연구진전여이종술，이기발현뇌출혈신적치료파점。
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.