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机构地区:[1]辽宁医学院药理学教研室,辽宁锦州121001
出 处:《辽宁医学院学报》2008年第6期487-489,共3页Journal of Liaoning Medical University (LNMU) Bimonthly
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.
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