CAJ | 학술논문

脑缺血损伤发生机制十分复杂，目前有多种相关学说，大量研究表明炎症反应是脑缺血损伤主要机制之一，然而炎性瀑布反应触发后更加剧了脑损伤的发展，其中炎性受体发挥了重要作用。研究表明Toll样受体4(TLR4)在脑缺血的发生、发展和继发性脑损伤中起重要作用，髓样分化因子88(MyD88)是TLR4信号转导通路中关键的衔接蛋白，能够启动下游炎性因子的转导。对TLR4介导的MyD88信号通路在脑缺血损伤中的作用进展做一综述。
뇌결혈손상발생궤제십분복잡，목전유다충상관학설，대량연구표명염증반응시뇌결혈손상주요궤제지일，연이염성폭포반응촉발후경가극료뇌손상적발전，기중염성수체발휘료중요작용。연구표명Toll양수체4(TLR4)재뇌결혈적발생、발전화계발성뇌손상중기중요작용，수양분화인자88(MyD88)시TLR4신호전도통로중관건적함접단백，능구계동하유염성인자적전도。대TLR4개도적MyD88신호통로재뇌결혈손상중적작용진전주일종술。
Cerebral ischemic injury mechanism is very complex, there are a variety of related theories, a large number of studies have shown that inlfammation is one of the main mechanisms of cerebral ischemic injury, but is exacerbated by the development of brain injury after triggering the inflammatory cascade, in which inflammatory receptors play an important role. Studies have shown that toll-like receptor 4 (TLR4) plays an important role in the development of secondary brain injury and cerebral ischemia, and myeloid differentiation factor 88 (MyD88) is TLR4 signal transduction pathway critical convergence protein, can start transduction downstream inlfammatory factors. The role of TLR4-mediated MyD88 signaling pathway in cerebral ischemic injury were reviewed.