C型凝集素受体参与出血性卒中炎性脑损伤的作用机制及前景展望 The Mechanism and Prospect of Mincle Receptor as a Therapeutic Target for Inflammatory Brain Injury of Hemorrhagic Stroke

Abstract

巨噬细胞诱导的C型凝集素（macrophage-inducible C-type lectin，Mincle）受体是模式识别受 体家族的重要成员，可以识别从坏死细胞中释放的自配体，并与下游的脾酪氨酸激酶（Spleen tyrosine kinase，Syk）作用激活单独信号通路，引发一系列炎性反应。越来越多的实验数据表明，Mincle/Syk信 号转导通路参与了包含卒中在内的多种神经系统疾病的炎症反应，特异性的抑制该通路激活可以抑 制神经炎症，修复神经功能损伤。本文主要对Mincle作用机制和病理研究进展进行综述，并对Mincle 对出血性卒中的治疗作用进行展望。 Abstract: pattern recognition receptors, can identify the release from a dead cells from the ligand, activate downstream of the spleen tyrosine kinase (Syk) signal path alone, and cause a series of inflammatory reaction.More and more studies shows that as the Mincle/Syk signaling pathway participate in the inflammatory response to a variety of neurological diseases including stroke, inhibit the activation of this pathway can prevent nerve inflammation and improve neurological damage. This review is to summarize the essential mechanisms and pathological progress about Mincle/Syk in hemorrhagic stroke and highlight the prospective possibility of applying these approaches in ICH therapy strategy.

Keywords

• c型凝集素
• mincle/syk
• card9
• 出血性卒中
• 神经炎症
• c-type lectin
• hemorrhagic stroke
• neuroinflammation