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在中枢神经系统中干扰素(interferon,IFN)信号系统的激活通常与炎症相关。但是,在肌萎缩性侧索硬化症(amyotrophic lateral sclerosis,ALS)动物模型SOD1(G93A)小鼠的脊髓中,症状前阶段I型IFN激活基因(IFN-stimulated genes,ISGs)的高度激活可在没有明显炎症的情况下发生。为了确定同样的信号系统是否在其它神经损伤中也有增强,我们检测了一种IFN激活基因ISG15在急性和慢性神经损伤的小鼠模型中的蛋白表达水平。我们观察到ISG15蛋白在经受全脑缺血或创伤性脑损伤的小鼠以及过度表达HIV gp120蛋白的转基因小鼠的大脑中显著增加。以上结果提示,ISGs的激活是神经损伤的一种普遍特性,并且ISG15可成为一种适用于检测中枢神经系统神经损伤的生物标志。
Activation of the interferon (IFN) signaling system in the central nervous system is usually associated with inflammation. However, in the spinal cord of the SOD1 (G93A) mouse model of amyotrophic lateral sclerosis (ALS) animal model, the high activation of pre-symptomatic IFN-stimulated genes (ISGs) No obvious inflammation occurred in the case. To determine whether the same signaling system was also enhanced in other neurological damage, we examined the protein expression of an IFN-activated gene, ISG15, in mouse models of acute and chronic neuronal injury. We observed a significant increase of ISG15 protein in the brains of mice that underwent global cerebral ischemia or traumatic brain injury as well as transgenic mice overexpressing HIV gp120 protein. The above results suggest that activation of ISGs is a common feature of nerve injury and that ISG15 may be a biomarker suitable for detecting nerve damage in the central nervous system.