Clark W M, Lutsep H L
Oregon Stroke Center, Dept. of Neurology UHS44, Oregon Health Sciences University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97201, USA.
Expert Opin Biol Ther. 2001 Mar;1(2):227-37. doi: 10.1517/14712598.1.2.227.
Central nervous system (CNS) ischaemia is associated with an acute inflammatory response which appears to potentiate CNS injury, especially following reperfusion. This response includes the release of inflammatory mediators called cytokines including IL-1 and TNF-alpha, which triggers the production of additional cytokines including IL-6 and activates leukocytes which infiltrate into the CNS. Increased expression of cytokines has been demonstrated to occur in the first few hours after CNS ischaemia. Preliminary clinical studies suggest that plasma levels of IL-6 are correlated with functional recovery while brain levels of cytokines have been demonstrated to increase following experimental ischaemia. Although there are no current clinical 'anti-cytokine' treatment studies for stroke, experimental studies modulating IL-1 and TNF-alpha have shown neuroprotection.
中枢神经系统（CNS）缺血与急性炎症反应相关，这种反应似乎会加重中枢神经系统损伤，尤其是在再灌注后。这种反应包括称为细胞因子的炎症介质的释放，包括白细胞介素-1（IL-1）和肿瘤坏死因子-α（TNF-α），它们会触发包括白细胞介素-6（IL-6）在内的其他细胞因子的产生，并激活浸润到中枢神经系统的白细胞。细胞因子的表达增加已被证明在中枢神经系统缺血后的最初几个小时内就会出现。初步临床研究表明，IL-6的血浆水平与功能恢复相关，而在实验性缺血后，细胞因子的脑内水平已被证明会升高。虽然目前尚无针对中风的临床“抗细胞因子”治疗研究，但调节IL-1和TNF-α的实验研究已显示出神经保护作用。
