期刊文献+

卡维地洛及TNF-α对内皮细胞释放t-PA和PAI-1的影响 被引量:5

THE EFFECTS OF CARVEDILOL AND TNF-α ON ENDOTHELIAL CELL SECRETING t-PA AND PAI-1
下载PDF
导出
摘要 目的 研究卡维地洛及肿瘤坏死因子α(TNF α)对内皮细胞分泌组织纤溶酶原激活物 (t PA)和纤溶酶原激活物抑制剂 1(PAI 1)的影响。方法 培养内皮细胞株 (ECV3 0 4) ,分为TNF α刺激组 ,培养基中TNF α加至终浓度为 5、10、2 5、5 0、10 0ng/ml;卡维地洛干预组 ,培养基中加TNF α (5 0ng/ml)后加入卡维地洛 ,终浓度为 2 0、5 0、10 0、2 0 0nmol/L ,2 4h后测定上清中的组织纤溶酶原激活物 (t PA)和纤溶酶原激活物抑制剂 1(PAI 1)的含量。结果 内皮细胞在TNF α刺激 2 4h后 ,其分泌的PAI 1抗原含量与对照组比有明显升高 ,有显著性差异 (P <0 0 5 ) ,而两组间t PA含量无明显差异 (P >0 0 5 )。而卡维地洛干预组却显著降低PAI 1(P <0 0 5 ) ,对t PA含量无明显作用 (P >0 0 5 )。结论 TNF α对内皮细胞株分泌的PAI 1有显著的升高作用 ,而对t PA无显著影响 ;用卡维地洛干预后 ,PAI 1显著降低 ,t PA含量无明显改变。 Objective: To investigate the effects of tumor necrosis factor Alpha(TNF?α) and carvedilol on endothelial cell secreting tissue plasminogen activator(t?PA) and plasminogen activator inhibitor (PAI?1). Methods: Cultivated ECV304 cells were stimulated with TNF?α(5? 10? 25? 50? 100 ng/ml)or TNF?α plus carvedilol(20? 50? 100? 200 nmol/L)for 24 h. Tissue?type plasminogen activator (t?PA) and plasminogen activator inhibitor?1 (PAI?1) in the supernatant of the cell culture were measured by enzyme linked immunosorbent assay (ELISA). Results: The concentrations of t?PA had no statistically significant changes whether the ECV304 cells were stimulated by TNF?α or carvedilol.But PAI?1 was significantly increased by TNF?α and decreased by carvedilol. Conclusions: TNF?a and carvedilol have no effect on t?PA released from ECV304, but PAI?1 can be increased by TNF?α and decreased by carvedilol . TNF?α or carvedilol plays a role in the regulating of fibrinolysis.
出处 《实用临床医药杂志》 CAS 2003年第5期448-449,452,共3页 Journal of Clinical Medicine in Practice
关键词 卡维地洛 肿瘤坏死因子Α 内皮细胞 组织纤溶酶原激活物 carvedilol tumor necrosis factor Alpha (TNF-α) endothelial cell tissue plasminogen activator (t-PA) plasminogen activator inhibitor-1(PAI-1)
  • 相关文献

参考文献7

  • 1van Mourik J A, Lawrence D A, Loskutoff D J. Purification of an inhibitor of plasminogen activator (antiactivator) synthesized by endothelial cells[J]. J Biol Chem, 1984, 259(23):1491.
  • 2Vallet B, Wiel E. Endothelial cell dysfunction and coagulation[J]. Critical Care Medicine, 2001, 29(7 Suppl) : S36.
  • 3Rossig L, Haendeler J, Mallat Z. Congestive heart failure induces endothelial cell Apotosis; protective role of carvedilol[ J ].J Am Coll Cardiol, 2000, 36(7): 2081.
  • 4Soeda S, Tsunoda T, Kurokawa Y, et al. Tumor necrosis factor-α-induced release of plasminogen activator inhibitor-1 from human umbilical vein endothelial cells: involvement of intracellular ceramide signaling event [ J ]. Biochimica et Biophysic aActa, 1998, 1448(1): 37.
  • 5Birgel M, Gottschling-Zeller H, Rhrig K, et al. Role of cytokines in the regulation of plasminogen activator inhibitor-1 expression and secretion in newly differentiated subcutaneous human adipocytes[J ]. Arteriosclerosis, Thrombosis, and Vascular Biology, 2000, 20(6): 1682.
  • 6Shimokawa T, Yamamoto K, Kojima T, et al. Down-regulation of murine tissue factor pathway inhibitor mRNA by endotoxin and tumor necrosis factor-α in vitro and in vivo [J].Thrombosis Research, 2000, 100(3): 211.
  • 7Polte T, Oberle S, Sehder H. Nitric oxide protects endothelial cells from turmornecrosis factor-α-mediated cytotoxicity: Possible involvment of cyclic-GMP[J]. FEBS Lett, 1997, 409(1): 46.

同被引文献29

引证文献5

二级引证文献48

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部