CAJ | 학술논문

目的研究局部脑缺血模型小胶质细胞的激活和白细胞的浸润情况,以进一步研究脑卒中后引起炎症反应的细胞及分子机制.方法用免疫组化方法研究单克隆抗体CD11b,Ly-6G,CD3和CD45/B220在大脑中动脉闭塞(MCAO)60 min进行不同时段灌注后在脑组织中的表达.结果灌注早期(18～24 h)在脑梗塞区就可见被激活的CD11b阳性的小胶质细胞,在18～24 h灌注期,可见CD11b阳性的巨噬细胞和Ly-6G阳性的中性白细胞黏附在脑膜的血管壁.灌流48～72 h,CD11b阳性的巨噬细胞和Ly-6G阳性的中性白细胞从血管壁迁移到脑梗塞区.在灌流24～48 h,我们仅见到个别CD3阳性T淋巴细胞和CD45/B220阳性B淋巴细胞.然而,在灌流72 h后,可容易地检测到CD3阳性T淋巴细胞.结论研究结果表明单核吞噬细胞系统在MCAO脑卒中模型的炎症反应中起重要作用.在灌注早期CD11b阳性细胞主要为脑实质内被激活的小胶质细胞,灌注24～72 h,外周血循环中的巨噬细胞和其他白细胞从血管迁移到缺血区以及被激活的小胶质细胞一同在脑卒中炎症反应中起作用.
목적연구국부뇌결혈모형소효질세포적격활화백세포적침윤정황,이진일보연구뇌졸중후인기염증반응적세포급분자궤제.방법용면역조화방법연구단극륭항체CD11b,Ly-6G,CD3화CD45/B220재대뇌중동맥폐새(MCAO)60 min진행불동시단관주후재뇌조직중적표체.결과관주조기(18～24 h)재뇌경새구취가견피격활적CD11b양성적소효질세포,재18～24 h관주기,가견CD11b양성적거서세포화Ly-6G양성적중성백세포점부재뇌막적혈관벽.관류48～72 h,CD11b양성적거서세포화Ly-6G양성적중성백세포종혈관벽천이도뇌경새구.재관류24～48 h,아문부견도개별CD3양성T림파세포화CD45/B220양성B림파세포.연이,재관류72 h후,가용역지검측도CD3양성T림파세포.결론연구결과표명단핵탄서세포계통재MCAO뇌졸중모형적염증반응중기중요작용.재관주조기CD11b양성세포주요위뇌실질내피격활적소효질세포,관주24～72 h,외주혈순배중적거서세포화기타백세포종혈관천이도결혈구이급피격활적소효질세포일동재뇌졸중염증반응중기작용.
Objective To identify microglial activation and leukocyte infiltration in focal cerebral ischemia for further research on the cellular and molecular mechanisms that lead to inflammation following stroke. Methods Immunocytochemistry (IHC) was used to investigate the expression of CD1 1b, Ly-6G, CD3 and CD45/B220 in cerebral ischemia induced by 60 min temporary occlusion of the middle cerebral artery followed by reperfusion for varying times. Results At early time points (18-24 h), resident CD11b + microglia appeared activated at the site of infarct. Peripheral CD11b +macrophages and Ly-6G + neutrophils were observed adhering to meningial vascular walls at 18-24 h of reperfusion.CD1 1b + macrophages and Ly-6G + neutrophils migrated from vessel walls into the parenchyma of the infarct following 48-72 h reperfusion. Minimal numbers of CD3 + T lymphocytes and CD45/B220 + B lymphocytes were detected at 24-48 h reperfusion. However, following 72 h reperfusion, CD3 + T lymphocytes were readily detected. Conclusion The data indicate that the mononuclear phagocytic system plays an important role in the inflammatory response following ischemic injury. The early inflammatory response cell appears to be primarily activated microglia, and around 24-72 h peripheral macrophages with other leukocytes from the circulation migrate into the ischemic site contributing to inflammatory response in stroke.