CAJ | 학술논문

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.
용결양-복양배경화흥강성안기산곡안산유도배양신경원세포손상화배사,관찰아나백체소(1)대체외배양대서뇌신경원세포배사적보호작용,이연구기항결혈성뇌손상적작용궤제.결과표명,1적3개제량조(25、50、100μg/ml)균능명현감경결양-복양소치적신경원세포손상,농도효응정정상관.정성관찰표명,1적3개제량조대곡안산치신경원세포손상역유개선작용,차여농도상관.제시재결양-복양화흥강성안기산도치적대서신경원세포손상중가능유IL-1염증통로삼여.
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 antiischemic brain injury.The results showed that three dosages of anakinra(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.