论文部分内容阅读
业已显示,内皮诱导的一氧化氮(NO)及其前身L-精氨酸可以促进血管生成,但对其精确机理现了解甚少.N-氮-L-精胺酸乙酯(L-NAME,1mmo/L)能抑制内源性的NO生成,进而抑制家牛主动脉内皮单层细胞边缘的内皮细胞胚芽,而其非活性的对映体D-NAME(1mmol/L)则不能抑制内源性的NO生成.L-NAME能抑制内源性的NO释放,已由NO专用电极通过安培计测量得到证实.在改进的Boyden舱内,L-NAME(1mmol/L)能显著地抑制内皮细胞的迁移.但根据[a~3H]胸腺嘧啶核甙混合物分析评价,L-NAME并不影响内皮DNA的合成.然后,我们用L-NAME在人体脐静脉内皮细胞中抑制NO,并检测内皮细胞粘着分子表达式的变化.在正常氧和低氧环境中,L-NAME(1mmol/L)能抑制粘合家分子,αvβ_3的表面表达.αvβ_3是促进内皮细胞存活和血管生成的一种重要的粘合素分子.然而,L-NAME并不影响血小板内皮细胞粘着分子-1,细胞间粘着分子-1,血管内皮粘着分子-1,间隙连接蛋白43,以及VE-钙粘附因子的表达,据报道这些分子可能影响血管生成.总之,L-NAME抑制内皮NO合酶可以减离体内皮细胞的迁移,但不能使其增生,进而,内源性内皮诱导的NO能维持粘合素分子αvβ_3的功能表达,αvβ_3是内皮迁移、存活和血管生成的递质.所以,内皮诱导的NO通过粘合素因子依赖机制,在支持内皮细胞迁移和
Endothelial-induced nitric oxide (NO) and its predecessor L-arginine have been shown to promote angiogenesis, but little is known about their precise mechanisms. N-Nitro-L-arginine ethyl ester , 1 mmo / L) inhibited endogenous NO production, which in turn inhibited the endothelial cell germ in the bovine aortic endothelium monolayer, whereas the inactive enantiomer D-NAME (1 mmol / L) L-NAME can inhibit the release of endogenous nitric oxide, which has been confirmed by the measurement of ammeter with NO special electrode. In the modified Boyden chamber, L-NAME (1mmol / L) can significantly inhibit the endothelium Cell migration, but L-NAME did not affect the synthesis of endothelial DNA according to the analysis of [a ~ 3H] thymidine mixture.We then used L-NAME to inhibit NO in human umbilical vein endothelial cells L-NAME (1mmol / L) can inhibit the expression of adhesive molecules and αvβ_3 in normal oxygen and hypoxia environment.αvβ_3 is an important factor to promote endothelial cell survival and angiogenesis However, L-NAME did not affect platelet adhesion molecule-1, intercellular adhesion molecule-1, vascular endothelial Adhesion Molecule-1, Glitrelin 43, and VE-cadherin expression, these molecules are reported to affect angiogenesis. In conclusion, L-NAME inhibits endothelial NO synthase loss from endothelial cell migration but not And then proliferate, and then endogenous endothelial-induced NO maintains the functional expression of the integrin αvβ_3, which is the transmitter of endothelial migration, survival and angiogenesis.Thus, endothelium-induced NO is activated by the Adrenoghlin-dependent mechanism , In supporting endothelial cell migration and