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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:细胞原代培养成功后,运用免疫荧光实时测定星形胶质细胞及C6胶质瘤细胞在缓激肽作用前后的细胞内钙离子变化。结果:1×10-6mol/L BK作用于大鼠C6胶质瘤细胞后出现1个宽广的细胞内钙离子升高期,较长的(>30 s)钙离子波峰的升高期,高峰后存在明显的平台持续期,二次高峰多见,50%的钙离子升高持续时间较长(>50 s);进一步的研究显示,C6胶质瘤细胞上存在功能性的尼诺丁敏感受体,小剂量缓激肽可以引起肿瘤细胞内的钙离子水平升高,特别是首次刺激可以选择性引起尼诺丁受体介导的细胞内钙库释放。结论:首次小剂量缓激肽可以选择性触发C6胶质瘤细胞内的细胞内钙库释放,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所在。
OBJECTIVE: To explore the underlying mechanism of small dose bradykinin selective opening of blood tumor barrier. Methods: After the primary cultured cells were successfully cultured, the changes of intracellular calcium in astrocytes and C6 glioma cells before and after bradykinin were detected by immunofluorescence. Results: After a dose of 1 × 10-6 mol / L BK was administered to rat C6 glioma cells, there was a wide range of intracellular calcium rise, a long (> 30 s) rise and peak of calcium ion peak There was a clear platform duration after the second peak more common, 50% of calcium increased longer duration (> 50 s); further studies have shown that C6 glioma cells have functional nindenine sensitivity Receptors, low-dose bradykinin can cause elevated levels of calcium in tumor cells, especially the first stimulation can selectively lead to nicotine receptor-mediated intracellular calcium release. CONCLUSIONS: The first low-dose bradykinin selectively triggers the release of intracellular calcium from C6 glioma cells, which may be the reason that small doses of bradykinin selectively open the blood-tumor barrier.