Machein U, Lieb K, Hüll M, Fiebich B L
Psychiatrische Klinik, Universität Freiburg, Germany.
Neuroreport. 1995 Nov 27;6(17):2283-6. doi: 10.1097/00001756-199511270-00004.
Cytokines such as interleukin-1 (IL-1) and interleukin-6 (IL-6) have previously been shown to participate in neurodegenerative processes including Alzheimer's disease. However, the molecular consequences of increased cytokine expression in the brain remain largely unknown. We have studied the effects of IL-1, IL-6 and TNF alpha on the expression of the acute-phase protein alpha 1-antichymotrypsin (ACT) in human astrocytoma cell lines. Both IL-1 and TNF alpha, but not IL-6, were able to induce ACT gene transcription and protein synthesis. The synthetic glucocorticoid dexamethasone enhanced cytokine-induced ACT mRNA expression and protein synthesis. We conclude that IL-1-induced expression of ACT may be part of the inflammatory response in the brain and may be involved in the pathology of Alzheimer's disease.
诸如白细胞介素-1(IL-1)和白细胞介素-6(IL-6)等细胞因子先前已被证明参与包括阿尔茨海默病在内的神经退行性过程。然而,大脑中细胞因子表达增加的分子后果在很大程度上仍不清楚。我们研究了IL-1、IL-6和肿瘤坏死因子α(TNFα)对人星形细胞瘤细胞系中急性期蛋白α1-抗糜蛋白酶(ACT)表达的影响。IL-1和TNFα均能诱导ACT基因转录和蛋白质合成,而IL-6则不能。合成糖皮质激素地塞米松增强了细胞因子诱导的ACT mRNA表达和蛋白质合成。我们得出结论,IL-1诱导的ACT表达可能是大脑炎症反应的一部分,并且可能参与阿尔茨海默病的病理过程。