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目的:探讨Apelin-13对非对称性二甲基精氨酸(asymmetrical dimethyl arginine,ADMA)所致的人脐静脉内皮细胞(human umbilical endothelial cell,HUVEC)细胞骨架损害是否有保护作用及其可能的机制。方法:体外培养HUVEC,根据培养液中加入不同的药物分为正常对照组、ADMA 100μmol/L组、Apelin-13 10-6 mol/L组、Apelin-13 10-7 mol/L组、Apelin-13 10-8 mol/L组、ADMA(100μmol/L)+Apelin-13(10-6 mol/L)组、ADMA(100μmol/L)+Apelin-13(10-7 mol/L)组和ADMA(100μmol/L)+Apelin-13(10-8 mol/L)组,孵育24 h后,测量细胞骨架成分肌动蛋白(F-actin)、黏着斑蛋白(vinculin)含量,并测定细胞上清液一氧化氮(nitric oxide,NO)的含量。结果:1)ADMA 100μmol/L单独作用可诱导人脐静脉内皮细胞F-actin和vinculin形成,细胞上清液的NO含量显著减少(P<0.01)。2)联合给予Apelin-13可以减少ADMA诱导的F-actin和vinculin的增加,增加细胞上清液中的NO含量(P<0.01)。3)相关性分析显示上清液中的NO含量分别与F-actin和vinculin含量呈负相关(r=-0.809,P<0.05;r=-0.781,P<0.05)。结论:Apelin-13能够减弱ADMA诱导的人脐静脉内皮细胞骨架损害,这一作用可能与NO生成增加有关。
Objective: To investigate whether Apelin-13 can protect human umbilical endothelial cell (HUVEC) cytoskeleton induced by asymmetric dimethyl arginine (ADMA) and its possible mechanism mechanism. Methods: HUVECs were cultured in vitro and divided into normal control group, ADMA 100μmol / L group, Apelin-13 10-6 mol / L group, Apelin-13 10-7 mol / L group, Apelin- The ADMA (100μmol / L) + Apelin-13 (10-6 mol / L), ADMA (100μmol / L) + Apelin-13 (100 μmol / L) and Apelin-13 (10-8 mol / L) for 24 h. The levels of F-actin and vinculin in the cytoskeleton were measured, Nitric oxide (NO) content. Results: 1) ADMA alone at 100 μmol / L induced the formation of F-actin and vinculin in human umbilical vein endothelial cells, and the NO content in the supernatant decreased significantly (P <0.01). 2) Combined administration of Apelin-13 could reduce ADMA-induced increase of F-actin and vinculin and increase NO content in supernatant (P <0.01). 3) Correlation analysis showed that the content of NO in supernatant was negatively correlated with the content of F-actin and vinculin respectively (r = -0.809, P <0.05; r = -0.781, P <0.05). Conclusion: Apelin-13 can attenuate ADMA-induced injury of human umbilical vein endothelial cells, which may be related to the increased production of NO.