Toll样受体2在缺血性脑损伤中的作用机制研究进展

Recent advance in mechanism of Toll-like receptor 2 in cerebral ischemic injury

缺血性脑损伤的发生机制极其复杂，大量研究表明炎症反应是其主要机制之一。炎性瀑布反应触发并加剧了缺血性脑损伤的发展，其中炎性受体发挥了重要作用。实验研究表明Toll样受体2（TLR2）在缺血性脑损伤的发生、发展和继发性脑损伤中可能起重要作用。髓样分化因子88（MyD88）是TLR2信号传导通路中关键的衔接蛋白，能够启动下游炎性因子的传导，而Mvd88主要参与对核转录因子-κB（NF-κB）DNA结合活性的调控。本文就TLR2介导的MyD88信号传导通路在缺血性脑损伤中的可能作用机制进行综述，希望能够以TLR2和MyD88作为信号传导通路中的核心环节，成为药物靶向治疗的研究对象，为减轻缺血性脑损伤提供新的对策。

The mechanism of cerebral ischemic injury is very complex. A lot of studies have shown that inflammatory reaction is one of the main mechanisms of cerebral ischemic injury, and the inflammatory response of the waterfall is more important. Experimental studies show that Toll like receptor 2 （TLR2） may play an important role in the initiation and development of cerebral ischemia, and may lead to the secondary brain injury. Myeloid differentiation factor 88 （MyD88） is the key of the TLR2 signal transduction pathway, which can activate the downstream inflammatory factors. And myd88 is mainly involved in the regulation ofNF-KB DNA binding activity. The role of MyD88 signaling pathway mediated by TLR2 is reviewed in cerebral ischemic injury in this paper. MyD88 is the key link in the signal transduction pathway, which can be used as the research object of drug targeting therapy.