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目的旨在观察TMB8对血管内皮细胞[Ca2+]i水平和NO释放的影响,探讨扩张脑血管的机制。用ARCMMIC阳离子测定系统,测量单个细胞内游离钙浓度([Ca2+]i),用血红蛋白法测量一氧化氮(NO)的释放。结果表明,在细胞外钙浓度为13mmol·L-1时,TMB8125及250μmol·L-1对静息[Ca2+]i和甲基血红蛋白ΔE无明显影响,而50及100μmol·L-1时可升高静息[Ca2+]i和甲基血红蛋白ΔE。表明TMB850及100μmol·L-1升高脑血管内皮[Ca2+]i,激活NO合酶,促进NO合成和释放,这可能是其扩张脑血管的重要机制之一。
Purpose To observe the effect of TMB8 on [Ca2 +] i level and NO release in vascular endothelial cells and to explore the mechanism of dilation of cerebral blood vessels. The system was used to measure the intracellular free calcium concentration ([Ca2 +] i) with the AR-CM-MIC cation assay and the release of nitric oxide (NO) was measured by the hemoglobin method. The results showed that TMB8125 and 250μmol·L-1 had no significant effect on the resting [Ca2 +] i and methyl hemoglobin ΔE when the extracellular calcium concentration was 13mmol·L-1, 100μmol·L-1 increased resting [Ca2 +] i and methyl hemoglobin ΔE. These results suggest that TMB850 and 100μmol·L-1 elevate [Ca2 +] i in cerebrovascular endothelium, activate NO synthase and promote NO synthesis and release, which may be one of the important mechanisms of its expansion of cerebrovascular.