Institute of Nursing and Health, Henan University, Kaifeng 475004, China.
School of Clinical Medicine, Henan University, Kaifeng 475004, China.
Cells. 2022 Nov 26;11(23):3781. doi: 10.3390/cells11233781.
Subarachnoid hemorrhage (SAH) is one of the common clinical neurological emergencies. Its incidence accounts for about 5-9% of cerebral stroke patients. Even surviving patients often suffer from severe adverse prognoses such as hemiplegia, aphasia, cognitive dysfunction and even death. Inflammatory response plays an important role during early nerve injury in SAH. Toll-like receptors (TLRs), pattern recognition receptors, are important components of the body's innate immune system, and they are usually activated by damage-associated molecular pattern molecules. Studies have shown that with TLR 4 as an essential member of the TLRs family, the inflammatory transduction pathway mediated by it plays a vital role in brain injury after SAH. After SAH occurrence, large amounts of blood enter the subarachnoid space. This can produce massive damage-associated molecular pattern molecules that bind to TLR4, which activates inflammatory response and causes early brain injury, thus resulting in serious adverse prognoses. In this paper, the process in research on TLR4-mediated inflammatory response mechanism in brain injury after SAH was reviewed to provide a new thought for clinical treatment.
蛛网膜下腔出血(SAH)是常见的临床神经系统急症之一。其发病率约占脑卒中患者的 5-9%。即使幸存的患者,也常遭受严重的不良预后,如偏瘫、失语、认知功能障碍,甚至死亡。炎症反应在 SAH 早期神经损伤中起着重要作用。Toll 样受体(TLRs)是模式识别受体,是机体固有免疫系统的重要组成部分,通常由损伤相关分子模式分子激活。研究表明,以 TLR4 作为 TLRs 家族的重要成员,其介导的炎症转导途径在 SAH 后脑损伤中起着至关重要的作用。SAH 发生后,大量血液进入蛛网膜下腔,可产生大量的损伤相关分子模式分子与 TLR4 结合,激活炎症反应,导致早期脑损伤,从而导致严重的不良预后。本文就 TLR4 介导的炎症反应机制在 SAH 后脑损伤中的研究进展作一综述,为临床治疗提供新的思路。