细胞因子、趋化细胞因子与脑缺血后炎症损伤  

The molecular mechanisms of inflammation following cerebral ischemia

作　　者：徐皓亮[1] 冯亦璞[1] 

机构地区：[1]中国医学科学院中国协和医科大学药物研究所

出　　处：《中国药理学通报》1999年第3期208-211,共4页Chinese Pharmacological Bulletin

摘　　要：阐明细胞因子、趋化细胞因子在脑缺血后炎症发生中的作用。脑缺血区细胞具有免疫活性，可分泌多种免疫介质，促进外周白细胞进入受损脑区，致使炎症的发生。细胞因子是这一过程中的关键因子，且通过多种途径和趋化细胞因子、粘附分子共同启动和调节炎症的发生发展过程。这些介质在脑缺血中的表达具有一定的时间依赖性。了解脑缺血后细胞因子化学因子的级联反应，对寻找减轻脑缺血后继发性损伤的新途径具有重要的意义。To elucidate the mechanisms of brain inflammation, and shed light on the causes of secondary brain damage following cerebral ischemia. In infarct region, brain cells have been shown to become immunologically reactive and interact with each other by producing various substances including cytokines and chemokines. Cytokines and chemokines have been revealed to be the primary mediators that work in concert with other molecules to initiate and regulate the local inflammation following cerebral ischemia. They promote the inflammation process, possibly by attracting or modulating inflammation cells in the ischemic area. The induction of these molecules in ischemic brain is time locked and appears to be regulated by a complex network elicited by ischemic insults. Understanding this cytokine chemokine interaction cascade in the ischemic brain is very important to find a way of controlling those key mediators to attenuate the secondary brain damage.

关 键 词：脑缺血 炎症 细胞因子 趋化细胞因子 

分 类 号：R743.310.2[医药卫生—神经病学与精神病学]