CAJ | 학술논문

目的检测Th17细胞在缺血脑组织中的表达及其细胞因子IL-17在厌氧条件下对神经元损伤机制的研究.方法线栓法建立小鼠持续性大脑中动脉栓塞模型(pMCAO),免疫荧光技术检测pMCAO小鼠缺血侧脑组织中Th17细胞的表达；体外原代培养新生小鼠海马神经元,建立体外氧糖剥夺模型(OGD)模拟体内脑缺血缺氧微环境,观察不同厌氧时间对神经元的损伤作用,同时进行不同浓度的IL-17干预以及IL-17受体(IL-17R)封闭实验,探讨IL-17在厌氧条件下对神经元损伤过程中的作用.结果成功建立小鼠右侧大脑中动脉栓塞模型,HE染色可见患鼠缺血侧脑组织空洞坏死样改变并有大量淋巴细胞浸润,TTC染色呈现白色缺血灶.免疫荧光染色可见缺血灶周边大量Th17细胞(CD4+IL-17+).体外实验中,外源性IL-17的干预加剧了OGD条件对海马神经元的损伤作用,并且这种作用能够被IL-17 R封闭剂所抑制.结论小鼠缺血脑组织中存在Th17细胞的浸润,Th17细胞分泌的IL-17与厌氧条件下神经元的损伤有关.
목적 검측Th17세포재결혈뇌조직중적표체급기세포인자IL-17재염양조건하대신경원손상궤제적연구.방법 선전법건립소서지속성대뇌중동맥전새모형(pMCAO),면역형광기술검측pMCAO소서결혈측뇌조직중Th17세포적표체；체외원대배양신생소서해마신경원,건입체외양당박탈모형(OGD)모의체내뇌결혈결양미배경,관찰불동염양시간대신경원적손상작용,동시진행불동농도적IL-17간예이급IL-17수체(IL-17R)봉폐실험,탐토IL-17재염양조건하대신경원손상과정중적작용.결과 성공건립소서우측대뇌중동맥전새모형,HE염색가견환서결혈측뇌조직공동배사양개변병유대량림파세포침윤,TTC염색정현백색결혈조.면역형광염색가견결혈조주변대량Th17세포(CD4+IL-17+).체외실험중,외원성IL-17적간예가극료OGD조건대해마신경원적손상작용,병차저충작용능구피IL-17 R봉폐제소억제.결론 소서결혈뇌조직중존재Th17세포적침윤,Th17세포분비적IL-17여염양조건하신경원적손상유관.
Objective To investigate the expression of Th17 in ischemic brain tissue and the mechanism of IL-17 in potentiating neuronal injury induced by oxygen-glucose deprivation.Methods Set up the permanent middle cerebral artery occlusion (pMCAO)model by an intraluminal nylon introduction.Investigate the Th17 cells in the ischemic brain tissue by immunofluorescence detection.oxygen-glucose deprivation (OGD) was induced in primary hippocampus cell cultures to modify ischemia microenvironment.Different dose of recombined IL-17 administration with or without IL-17R inhibitor was carried out to explore the mechanism of IL-17 in potentiating neuronal injury under OGD.Results Animal model of pMCAO was successfully set up with large cerebral infarctions after TTC stain.Infiltration of Th17 cells was observed according to the double-immunofluorescence for CD4 and IL-17.Exogenous IL-17 facilitated OGD-mediated neuronal cell death which could be blocked using IL-17R inhibitor.Conclusion There was Th17 cells infiltration in the ischemic brain of pMCAO mice.IL-17 secreted from Th17 cells was relevant to OGD-induced neuronal injury.