缓激肽选择性调节血肿瘤屏障的内在基础  

The basis for bradykinin's selective modulation of the blood tumor barrier

作　　者：丛雪枫[1] 王义宝[2] 刘云会[2] 

机构地区：[1]沈阳市第一人民医院神经外科,辽宁沈阳110041 [2]中国医科大学附属第一医院神经外科,辽宁沈阳110001

出　　处：《现代肿瘤医学》2006年第5期527-529,共3页Journal of Modern Oncology

基　　金：国家自然科学基金资助项目(No30070268)

摘　　要：目的体外探讨缓激肽的作用靶点细胞及缓激肽选择性开放血脑屏障的可能机制。方法免疫荧光测定脑血管内皮细胞、胶质细胞及C6细胞在不同剂量缓激肽作用前后的细胞内钙离子变化,WesternBlot测定3组细胞的缓激肽B2受体表达水平。结果小剂量缓激肽可以引起肿瘤细胞内的钙离子水平升高,而只有大剂量缓激肽才能触发星形胶质细胞内的钙离子水平变化,脑血管内皮细胞对大、小剂量缓激肽均无任何反应;3组细胞缓激肽B2受体的WesternBlotIDV(integrateddensityvalue)分别为5000.12±1110.21(n=2),18480.88±4119.86(n=3),63032.13±2802.71(n=4),组间比较有显著差异。结论缓激肽的直接作用靶点是星形胶质细胞及肿瘤细胞,两种细胞B2受体表达水平差异是小剂量缓激肽选择性开放血肿瘤屏障的物质基础;缓激肽可能通过某些细胞间信使来起到调节脑血管内皮细胞通透性的作用。Objective： To investigate in vitro the target cells for different doses of bradykinin （BK） and the underlying basis of BK that could selectively modulate the blood tumor/brain barrier. Methods： BK related intracellular calcium changes in astrocyte, C6 glioma cell and brain microvascular endothelial cell （BMEC） were studied respectively and Western blot analysis of B2 receptors was performed in the above three lines of cell. Results： Small dose of BK could trigger intracellular calcium elevation in C6 cell, whereas only large dose could do that to astrocyte, and the BMEC remained unresponsive to BK. Western blot results showed that the IDV of three lines of cell were 5000. 12 ± 1110.21 （ n = 2 ）, 18480.88 ± 4119.86 （ n = 3 ）, 63032.13 ± 2802.71 （ n = 4 ） respectively and there was a significant difference among the three lines of cell. Conclusion： The direct target cells of bradykinin are astrocyte and tumor cell, the unequal distribute of B2 receptors between them contributes to the ability of bradykinin that could selectively open the blood tumor barrier, relying on some intercellular messenger, bradykinin could modulate the per- meability enhancement of BMEC.

关 键 词：缓激肽 血脑屏障 脑微血管内皮细胞 

分 类 号：R739.41[医药卫生—肿瘤]