摘要
动物实验及临床研究均支持炎症反应参与缺血性脑损伤的理论,但炎症反应本身及其对缺血性脑损害的影响相当复杂。脑缺血后,在缺血损伤区有多种细胞因子表达及炎细胞浸润,构成了缺血性损伤向炎症性损伤转变的基础,最近研究较多的主要有白细胞、肥大细胞、白介素-1β(IL-1β)及肿瘤坏死因子(TNF)等。
In both clinical and animal experiments, it has been confirmed that the inflammation in brain is involved in the development of brain damage after the ischemia. However, the pro-inflammatory mechanism is extremely complicated. Recently, a growing number of reports indicates that many factors play their roles in the inflammation, such as leukocyte, interleukin-1β（ IL-1β）, tumor necrosis factor（TNF） and mast cells. They are released/presented in the region of cerebral ischemia and include both ischemic and secondary brain injury.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2006年第1期5-9,共5页
Chinese Pharmacological Bulletin
