维生素C对脂质过氧化损伤人脐静脉内皮细胞的保护作用

Protective Effects of Vitamin C on the Cultured Human Umbilical Vein Endothelial Cell Injured by Lipid Peroxidation

为探讨维生素C对脂质过氧化损伤人脐静脉内皮细胞的保护作用及其可能的分子作用机制 ,在铜离子诱发的低密度脂蛋白氧化修饰的基础上 ,造成内皮细胞的脂质过氧化损伤模型 ,测定细胞上清液中和细胞内乳酸脱氢酶的活性及其乙酰胆碱诱发的内皮型一氧化氮合酶活性及一氧化氮的生成量。结果发现 ,脂质过氧化物明显增加上清液中乳酸脱氢酶活性 (P <0 .0 1 ) ,增加细胞死亡率 (P <0 .0 1 ) ;同时它也抑制内皮型一氧化氮合酶的活性(P <0 .0 1 ) ,具有剂量 -依赖效应。应用不同剂量的维生素C(浓度为 1 0 0 μmol L和 30 0 μmol L)后 ,该效应明显减弱 ;内皮型一氧化氮合酶活性与一氧化氮生成量之间呈正相关 ,r值分别为 0 .9844(P <0 .0 1 )和 0 .880 2 (P <0 .0 5)。由此提示 ,脂质过氧化物能直接损伤内皮细胞 ,抑制内皮型一氧化氮合酶活性 ;

Aim To explore the protective effect of Vitamin C on the human umbilical vein endothelial cell (hUVECs) injured by lipid peroxidation and its probable mechanism. Methods Confluent hUVECs were incubated with Vitamin C for 24 h and consequently exposed to lipid peroxides induced by high concentration of Copper ions. Lactate dihydrogenase (LDH) activity was measured in cell medium and lysate. Endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) production induced by acetylcholine were assessed by endothelial nitric oxide synthase and nitric oxide kits. Results Lipid peroxides enhanced markedly LDH activity and decreased nitric oxide bioavailability via the inhibited eNOS activity (P<0.01). These effects were attenuated by administration of different dose Vitamin C (100 μmol/L, 300 μmol/L); the correlation between eNOS activity and NO production was significant (r=0.9844, P<0.01; r=0.8802, P<0.05, respectively). Conclusions Lipid peroxides could injury hUVECs and inhibit eNOS activity directly. Vitamin C might play a protective role in hUVECs injured by lipid peroxidation.