摘要
目的：探讨白细胞介素-1（Interleukin－1，IL－1）在神经兴奋毒性中的作用。方法：以培养的胚胎大鼠大脑皮层神经元为研究对象，用台盼蓝染色和扫描电镜观察了IL－1ra（IL-1受体拮抗剂）对谷氨酸诱导的培养神经细胞毒性的影响；用Northern印迹杂交观察了IL－1β对培养神经细胞NMDARI（NMDA受体Ⅰ型亚单位）mRNA表达的影响。结果；IL-1ra（mg/L）可明显抑制谷氨酸（0．5mmol/L）引起的神经细胞毒性作用；IL－1β在1～50u／ml浓度范围内可剂量依赖地促进NMDARImRNA表达，IL－1ra可阻断此效应。结论；内源性IL－1参与了谷氨酸诱导神经细胞毒性的病理过程，其作用机制之一可能是促进了NMDARImRNA的表达。
To study action of IL-1 involved in neurotoxicity. Methods: The effects of IL-1ra(IL-1 receptor antagonist, IL-1ra) on glutamate-induced neurotoxicity were examined using cultured ratcortical neurons with Trypan blue exclusion and scan electromicroscope. Meanwhile, effects of IL-1β onexpression of NMDAR1 mRNA were observed in cultures. Results: IL-1ra (1mg/L) may significantlyinhibit neuronal damage induced by glutamate at concentration of 0. 5 mmol/L F IL-1β dose-deppndentlypromoted expression of NMDAR1 mRNA in cultures at dose of 1～50 u/ml IL-1ra may reverse the action of IL-1β. Conclusion: Endogenous IL-1 mediates pathological procession of llPuronal damage induced by glutamate, and one possibility of IL-1 involved in neurotoxicity is to stimulate expression ofNMDAR1 mRNA
出处
《北京医科大学学报》
CSCD
1997年第1期38-39,42,共3页
Journal of Peking University(Health Sciences)
基金
国家自然科学基金!39670265
关键词
白细胞介素1
神经元
药物作用
谷氨酸
Inteuleukin 1/pharmacol Neurons/drug eff RNA, messengen/metab Glutamates
