Angiotensin-converting enzyme inhibitors attenuate propofol-induced pro-oxidative and antifibrinolytic effect in human endothelial cells

被引:6
|
作者
Wojewodzka-Zelezniakowicz, Marzena [1 ]
Gromotowicz-Poplawska, Anna [2 ]
Kisiel, Wioleta [2 ]
Konarzewska, Emilia [1 ]
Szemraj, Janusz [3 ]
Ladny, Jerzy Robert [1 ]
Chabielska, Ewa [2 ]
机构
[1] Med Univ Bialystok, Dept Emergency & Disaster Med, Bialystok, Poland
[2] Med Univ Bialystok, Dept Biopharm, Mickiewicza 2c Str, PL-15089 Bialystok, Poland
[3] Med Univ Lodz, Dept Med Biochem, Lodz, Poland
关键词
Human umbilical vein cells; quinaprilat; enalaprilat; propofol; fibrinolysis; nitric oxide; oxidative stress; PLASMINOGEN ACTIVATOR RELEASE; NITRIC-OXIDE; INSULIN-RESISTANCE; T-PA; EXPRESSION; QUINAPRIL; CAPTOPRIL; PATHWAY; TISSUE; HYPERTENSION;
D O I
10.1177/1470320316687197
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Introduction: The aim of this study was to investigate the effects of plasma and tissue angiotensin-converting enzyme inhibitors (ACE-Is) against propofol-induced endothelial dysfunction and to elucidate the involved mechanisms in vitro. Materials and methods: We examined the effects of propofol (50 mu M), quinaprilat and enalaprilat (10(-5) M) on fibrinolysis (t-PA, PAI-1, TAFI antigen levels), oxidative stress parameters (H2O2 and MDA antigen levels and SOD and NADPH oxidase mRNA levels) and nitric oxide bioavailability (NO2/NO3 concentration and NOS expression at the level of mRNA) in human umbilical vein endothelial cells (HUVECs). Results: We found that both ACE-Is promoted similar endothelial fibrinolytic properties and decreased oxidative stress in vitro. Propofol alone increased the release of antifibrinolytic and pro-oxidative factors from the endothelium and increased mRNA iNOS expression. We also found that the incubation of HUVECs in the presence of propofol following ACE-Is pre-incubation caused weakness of the antifibrinolytic and pro-oxidative potential of propofol and this effect was similar after both ACE-Is. Conclusions: This observation suggests that the studied ACE-Is exerted protective effects against endothelial cell dysfunction caused by propofol, independently of hemodynamics.
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页数:10
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