Utoguchi N, Ikeda K, Saeki K, Oka N, Mizuguchi H, Kubo K, Nakagawa S, Mayumi T
Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Osaka University, Japan.
J Cell Physiol. 1995 May;163(2):393-9. doi: 10.1002/jcp.1041630219.
The macromolecular permeability of cultured bovine aortic, bovine venous, and human umbilical vein endothelial cell monolayers was decreased significantly in culture medium containing L-ascorbic acid (Asc Acid; 0.01-0.1 mM) and L-ascorbic acid 2-phosphate (Asc 2-P). Dithiothreitol, which shows reducing activity equivalent to that of Asc Acid, did not affect endothelial permeability. Asc Acid induced a sixfold increase in collagen synthesis by the endothelial cells. The coexistence of L-azetidine 2-carboxylic acid, an inhibitor of collagen synthesis, attenuated the effect of Asc 2-P in a dose-dependent manner. Another collagen synthesis inhibitor, ethyl-3,4-dihydroxybenzoate, also inhibited collagen synthesis and increased endothelial permeability. The decrease in permeability of the endothelial monolayer was dependent on a reduction of the permeability coefficient of the endothelial monolayer. These findings indicate that endothelial barrier function is stimulated by Asc Acid via an increase in collagen synthesis.
在含有L-抗坏血酸（抗坏血酸；0.01-0.1 mM）和L-抗坏血酸2-磷酸酯（抗坏血酸2-磷酸酯）的培养基中，培养的牛主动脉、牛静脉和人脐静脉内皮细胞单层的大分子通透性显著降低。二硫苏糖醇的还原活性与抗坏血酸相当，但不影响内皮通透性。抗坏血酸使内皮细胞的胶原蛋白合成增加了六倍。胶原蛋白合成抑制剂L-氮杂环丁烷-2-羧酸的共存以剂量依赖的方式减弱了抗坏血酸2-磷酸酯的作用。另一种胶原蛋白合成抑制剂3,4-二羟基苯甲酸乙酯也抑制胶原蛋白合成并增加内皮通透性。内皮细胞单层通透性的降低取决于内皮细胞单层通透系数的降低。这些发现表明，抗坏血酸通过增加胶原蛋白合成来刺激内皮屏障功能。
