缓激肽对胶质瘤C6细胞NO释放的影响及意义  

Bardykinin triggers NO release in C6 glioma cells and its significance

作　　者：李连祥[1] 张洪亮[1] 王义宝[1] 

机构地区：[1]中国医科大学附属第一医院,沈阳110001

出　　处：《山东医药》2010年第30期3-5,共3页Shandong Medical Journal

基　　金：国家自然科学基金资助项目(30700249);沈阳市科学技术计划项目(1071206-1-00)

摘　　要：目的探讨小剂量缓激肽选择性开放血肿瘤屏障的内在机制。方法在缓激肽作用前后,分别采用NO荧光探针DAF-2/DA测定胶质瘤C6细胞内NO,观察缓激肽作用后的细胞间信号传导过程。结果缓激肽刺激可以引起C6细胞内继发于细胞内钙库释放后的NO水平升高;NO参与C6细胞至毗邻脑血管内皮细胞的信号传导过程。结论小剂量缓激肽可以触发C6细胞内钙库释放诱发的细胞内NO升高过程,这可能是小剂量缓激肽可以选择性开放血肿瘤屏障的原因。Objective To investigate the mechanism of bradykinin（BK） selectively modulate the blood-tumor barrier.Method The intracellular NO changes in C6 glioma cells was studied relying on the fluorescence of DAF-2/DA after BK was applied.Results BK could trigger long-lasting NO elevation which resulted from ryanodine mediated calcium store release,NO could diffused into adjacent brain microvascular endothelial cells which might be the underlying reason of BK modulation the permeability of brain microvascular endothelial cells.Conclusions Ryanodine mediated calcium release contributes to the long-lasting NO release after BK is applied,which might be the underlying reason of BK′s selective modulate the permeability of blood-tumor barrier.

关 键 词：胶质瘤 缓激肽 血肿瘤屏障 一氧化氮 

分 类 号：R739.41[医药卫生—肿瘤]