白介素17、白介素33在颅内动脉粥样硬化斑块中的作用及在缺血性卒中的展望

摘要

颅内血管粥样硬化会导致脑血管病,在颅内血管斑块的形成过程中以及缺血后的脑损伤中,炎症反应都起到至关重要的作用.近年来研究证实,白介素-17(interleukin-17,IL-17)与受体结合激活通路促进动脉粥样硬化斑块的形成,并且加重脑缺血组织的损伤,而白介素-33(interleukin-33, IL-33)在缺血性卒中通过IL-33/ST2L信号通路参与了颅内动脉硬化斑块的形成过程,且被证实是一种保护因素.本文总结了在颅内大血管硬化斑块的形成过程中IL-17与IL-33之间的相互影响.其各自水平的高低可反映疾病的严重程度,提出其对缺血性卒中的临床治疗及预示预后转归具有重要意义.%Cerebral vascular disease can be caused by intracranial atherosclerosis, during the formation of intracranial vascular plaques and post ischemic brain injury, and inflammation plays a crucial role. In recent years, studies have confirmed that interleukin 17 (IL-17) and the receptor activation pathway could promote the formation of atherosclerotic plaque and aggravate cerebral ischemia injury, and interleukin-33 (IL-33) got involved in the intracranial atherosclerotic plaques of ischemic stroke through IL-33/ST2L signaling pathway, which might be proved as a protective factor in atherosclerosis. This paper summarized mutual influence between IL-17 and IL-33 in the formation process of intracranial large artery atherosclerosis plaque. The level of their respective could reflect the severity of disease, which was of great significance to the clinical treatment and prognosis of ischemic stroke.