阿那白滞素对缺氧-复氧和兴奋性氨基酸所致神经细胞损伤的保护作用  

Protective Effects of Anakinra on Neuron Injury Induced by Hypoxia-reoxygenation and Excitatory Amino Acid

作　　者：夏玉叶[1] 盛雨辰[1] 钟雁[1] 李润平[2] 刘全海[1] 

机构地区：[1]上海医药工业研究院,上海200437 [2]第二军医大学药学院,上海200433

出　　处：《中国医药工业杂志》2010年第5期352-355,372,共5页Chinese Journal of Pharmaceuticals

摘　　要：用缺氧-复氧环境和兴奋性氨基酸谷氨酸诱导培养神经元细胞损伤和坏死,观察阿那白滞素(1)对体外培养大鼠脑神经元细胞坏死的保护作用,以研究其抗缺血性脑损伤的作用机制。结果表明,1的3个剂量组(25、50、100μg/ml)均能明显减轻缺氧-复氧所致的神经元细胞损伤,浓度效应呈正相关。定性观察表明,1的3个剂量组对谷氨酸致神经元细胞损伤亦有改善作用,且与浓度相关。提示在缺氧-复氧和兴奋性氨基酸导致的大鼠神经元细胞损伤中可能有IL-1炎症通路参与。The present study was designed to document the neuroprotective effects of anakinra on neuron injury induced by hypoxia-reoxygenation and excitatory amino acid--glutamic acid, then to explore its mechanism of anti- ischemic brain injury. The results showed that three dosages ofanakinra （25, 50, 100 μg/ml） could all obviously reduce neural cell damage induced by hypoxia-reoxygenation, and the effects had a direct correlation with concentration. The qualitative observation demonstrated that anakinra also could concentration-dependently protect neural cell from damage induced by excessive release of glutamic acid. The results suggested that the neuronal damage induced by hypoxiareoxygenation and excitatory amino acid might be mediated by IL-1 inflammatory pathway.

关 键 词：阿那白滞素 神经元细胞 缺氧-复氧 兴奋性氨基酸 谷氨酸 

分 类 号：R743[医药卫生—神经病学与精神病学]