氨氯地平对溶血磷脂酰胆碱致培养人脐静脉内皮细胞损伤的保护作用

①目的　探讨氨氯地平对溶血磷脂酰胆碱致培养人脐静脉内皮细胞损伤的保护作用。②方法　采用培养的人脐静脉血管内皮细胞 ,观察氨氯地平对溶血磷脂酰胆碱所致培养人脐静脉内皮细胞产生和分泌一氧化氮 (NO)及其合酶 (eNOS)、组织型纤溶酶原激活物 (t PA)、纤溶酶原激活物抑制物 (PAI 1)及乳酸脱氢酶活性变化的影响。③结果　溶血磷脂酰胆碱明显增加上清液中乳酸脱氢酶活性 ,提高细胞死亡率 ,增强PAI 1的活性 ,抑制eNOS及t PA的活性 ,与对照组比较差异有显著意义 (F =17.93～ 88.6 8,q =4 .0 1～ 2 0 .88,P <0 .0 5 )。而氨氯地平对溶血磷脂酰胆碱致培养人脐静脉内皮细胞损伤具有保护作用 (F =6 .34～ 11.2 2 ,q =5 .33～ 13.2 2 ,P <0 .0 5 )。④结论　氨氯地平对溶血磷脂酰胆碱致培养人脐静脉内皮细胞损伤具有保护作用

PROTECTIVE EFFECTS OF AMLODIPINE ON THE CULTURED HUMAN UMBILICAL VEIN ENDOTHELIAL CELL INJURED BY LYSOPHOSPHATIDYLCHOLINE

Objective To explore the protective effect of Amlodipine on the human umbilical vein endothelial cell ( HUVEC) injured by lysophosphatidylcholine. Methods Confluent HUVECs were incubated with Amlodipine for 24 h and subsequently exposed to lysophosphatidylcholine. Lactate dihydrogenase (LDH), plasminogen activator inhibitor-1 (PAI-1)and tissue plasminogen activator (t-PA) activity were measured in cell medium and lysate. Endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) production were assessed by endothelial nitric oxide synthase and nitric oxide kits. Results Lysophosphatidylcholine enhanced markedly PAI-1, LDH activity and cell death rate and decreased t-PA and eNOS activity ( F= 17.93- 88.68, q=4.01-20.88, P<0.05). These effects were attenuated by administration of different doses of Amlodipine(F= 6.34- 11.22, q=5.33-13.22, P<0.05). Conclusion Amlodipine might play a protective role in HUVECs injured by lysophosphatidylcholine.