Matsuo Y, Yamasaki Y, Kogure K
Developmental Research Laboratory, Shionogi & Co. Ltd., Osaka, Japan.
Keio J Med. 1996 Sep;45(3):270-4. doi: 10.2302/kjm.45.270.
Cytokines which promote emigration of leukocytes from the vascular lumen into the injured brain tissue are produced at the site of incipient cerebral infarction. The blood-borne invaders then accelerate the decomposition of brain cells by their toxic by-products, phagocytic action, and by the immune reaction. Recently accumulated data in our laboratories and other research facilities show that depleting the amount of circulating leukocytes or administering anti-inflammatory chemicals such as cytokine blocking agents, anti-adhesion molecule antibodies, and immunosuppressants effectively minimize the size of ischemia induced cerebral infarction. Based on the fact that leukocyte invasion of the affected brain tissue occurs 6 to 24 hours after onset of ischemia, administration of an anti-inflammatory therapy may widen the therapeutic window against stroke.
促进白细胞从血管腔迁移至受损脑组织的细胞因子在早期脑梗死部位产生。血行入侵者随后通过其毒性副产物、吞噬作用以及免疫反应加速脑细胞的分解。我们实验室和其他研究机构最近积累的数据表明，减少循环白细胞数量或给予抗炎化学物质，如细胞因子阻断剂、抗黏附分子抗体和免疫抑制剂，可有效减小缺血性脑梗死的面积。基于缺血发作后6至24小时受影响的脑组织会发生白细胞浸润这一事实，抗炎治疗可能会扩大中风的治疗窗口期。
