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出 处:《药学学报》1998年第9期650-654,共5页Acta Pharmaceutica Sinica
摘 要: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。The effect of 8-(N,N′-diethylamino)-n-octyl-3,4,5-trimethoxybenzoate(TMB-8) on [Ca^(2+)]i and the release of NO in cultured endothelial cells of the calf middle cerebral artery was studied by a system of measurement of AR-CM-MIC, using Fura2/AM as a fluoresent indicator and the oxyhaemoglobin method. In the presence of extracellular Ca^(2+) 13 mmol·L-1, the resting [Ca^(2+)]i and the extinction difference(ΔE) of between 401 and 410 nm were not changed by TMB8 125 and 25 μmol·L-1, but were increased by TMB8 50 and 100 μmol·L-1. The rise of ΔE induced by TMB8 50 and 100 μmol·L-1 was blocked completely by LNAME. The elevation of [Ca^(2+)]i was related to the release of NO. The result suggested that TMB8 increased resting [Ca^(2+)]i of endothelial cells of the calf middle cerebral artery and induced NO release.
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