Thorns Veronika, Walter Gerhard Franz, Licastro Federico
Department of Neuropathology, Medical School of Hannover, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany.
J Neuroimmunol. 2002 Jun;127(1-2):22-9. doi: 10.1016/s0165-5728(02)00072-3.
The interleukin-1beta (IL1beta) and interleukin-6 (IL6) have pro-inflammatory and neuroprotective functions and are elevated in many diseases of the brain. Here, mechanisms and effects of IL1beta and IL6 on neuronal survival after excitatory stimulation were investigated in vitro. IL6 upregulated the expression of the neuroprotective acidic fibroblast growth factor (aFGF) and reduced the glutamate-induced cytotoxicity. IL1beta treatment amplified the excitotoxic effects after 24 h, but longer treatment with IL1beta stimulated the neuronal release of IL6 resulting in increased levels of aFGF and a decreased excitotoxicity. These data suggest that (1) IL6 exerts protective functions by upregulating the expression of aFGF and (2) the IL6/IL1beta balance in the brain may regulate neuronal survival during neuropathological processes.
白细胞介素-1β（IL1β）和白细胞介素-6（IL6）具有促炎和神经保护功能，在许多脑部疾病中水平会升高。在此，我们在体外研究了IL1β和IL6对兴奋性刺激后神经元存活的机制和影响。IL6上调了神经保护性酸性成纤维细胞生长因子（aFGF）的表达，并降低了谷氨酸诱导的细胞毒性。IL1β处理24小时后会放大兴奋毒性作用，但更长时间的IL1β处理会刺激神经元释放IL6，导致aFGF水平升高和兴奋毒性降低。这些数据表明：（1）IL6通过上调aFGF的表达发挥保护作用；（2）大脑中的IL6/IL1β平衡可能在神经病理过程中调节神经元存活。
