摘要
目的:研究转换酶抑制剂卡托普利对内皮细胞组织型纤溶酶原激活物(t-PA)和纤溶酶原激活物抑制剂-1 (PAI-1)的影响。方法:培养肺静脉内皮细胞(ECV304),分别用肿瘤坏死因子(TNF)-α(浓度为5、10、25、50、100 μg/L)和血管紧张素Ⅱ(AngⅡ)(5、10、25、50、100 nmol/L)刺激,在50μg/L TNF-α刺激的基础上用卡托普利(20、50、100、200 nmol/L)共育,用ELISA的方法检测培养上清中的t-PA和PAI-1的浓度。结果:各浓度的TNF-α和AngⅡ刺激24 h后PAI-1的浓度明显增加,与空白对照相比P<0.05,而t-PA的差异则无统计学意义;各浓度的卡托普利明显抑制TNF-α(50μg/L)诱导的PAI-1分泌增多,P<0.05,而t-PA的变化不明显。结论:TNF-α和AngⅡ可以增加内皮细胞PAI-1的分泌,卡托普利可以抑制TNF-α诱导PAI-1的分泌,而t-PA则不受TNF-α、AngⅡ和卡托普利等因素影响。
Objective: To investigate the effects of captopril on fibrolytic balance. Methods: Cultivated ECV304 cells were stimulated with TNF-α(5,10,25,50,100 μg)and AngⅡ(5,10,25,50,100 nmol/L) for 24 hours. The same cells were also co-incubated with TNF-α(ng/ml)and captopril(20,50,100,200 nmol/L). Tissue-type plasminogen activator(t-PA) and plasminogen activator inhibitor-1 (PAI-1) in the supernatant were measured by enzyme linked immunosorbent assay (ELISA). Results: The concentrations of t-PA had no statistically significant changes in all supernatant of cultivated cells. But PAI-1 was significantly increased by Ang Ⅱ and TNF-α at same concentration. The PAI-1 secreting, induced by TNF-α, can be inhibited by captopril. Conclusion: Captopril has no effect on t-PA releasing from endo-thelial cells. TNF-α can increase PAI-1 secreting, but captopril can counteract this effect.
出处
《医学研究生学报》
CAS
2005年第B05期1-2,6,共3页
Journal of Medical Postgraduates
