摘要
目的探讨吡格列酮(pioglitazon,Pio)能抑制脂多糖(lipopolysaccharide,LPS)引起的培养大脑皮层神经元一氧化氮释放增加,并探讨其抑制作用信号转导机制。方法以体外培养6—7d的乳鼠大脑皮层神经元为研究对象,建立脂多糖损伤和吡格列酮保护模型。采用Griess法测定细胞培养上清液中NO含量。结果脂多糖可导致神经细胞损伤,培养液中NO含量升高;吡格列酮(1umol/L)可明显抑制脂多糖引起的NO含量的升高。结论吡格列酮可明显拮抗脂多糖诱导的神经细胞损伤。
Objective To explore the express effects of pioglitazon (Pio) on lipopolysaceharide - induced NO production to cultured cortical neurons and investigate its signaling pathway. Methods The inflammatory neurotoxicity model was constructed in primary cortical neurons isolated from Sprague - Dawley rats 6 - 7 d neonate rats following a dose lipopolysaccharide to the neurons directly. The contents of NO was detected. Results The cells, exposed to LPS ( 10 ug/mL for 8 h), showed charateristic change of damage, which could be relieved by pioglitazon (1umol/L) with cell survival rate increment. Pioglitazone could block the increase of NO induced by LPS. Condttsions Pioglitazone can prevent the neurons from the damage of LPS inflammatory neurotoxicity.
出处
《辽宁医学院学报》
CAS
2008年第6期487-489,共3页
Journal of Liaoning Medical University (LNMU) Bimonthly
关键词
吡格列酮
脂多糖
神经元
NO
pioglitazon
lipopolysaccharide
neurons
NO