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

Published on Jan 1, 2017in Journal of the Renin-Angiotensin-Aldosterone System1.356
· DOI :10.1177/1470320316687197
Marzena Wojewodzka-Zelezniakowicz6
Estimated H-index: 6
(UMB: Medical University of Białystok),
Anna Gromotowicz-Poplawska4
Estimated H-index: 4
(UMB: Medical University of Białystok)
+ 4 AuthorsEwa Chabielska16
Estimated H-index: 16
(UMB: Medical University of Białystok)
Abstract
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 μM), 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 weakn...
  • References (47)
  • Citations (2)
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References47
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#1Marzena Wojewodzka-Zelezniakowicz (UMB: Medical University of Białystok)H-Index: 6
#2Wioleta Kisiel (UMB: Medical University of Białystok)H-Index: 2
Last. Ewa Chabielska (UMB: Medical University of Białystok)H-Index: 16
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Angiotensin converting enzyme inhibitors and propofol both exert hypotensive action and may affect hemostasis. We investigated the influence of quinapril and propofol on hemodynamics and hemostasis in renal-hypertensive rats with induced arterial thrombosis. Two-kidney, one clip hypertensive rats were treated with quinapril (3.0 mg/kg for 10 days), and then received propofol infusion (15 mg/kg/h) during ongoing arterial thrombosis. The hemodynamic and hemostatic parameters were assayed. Quinapri...
7 CitationsSource
#1Zekuan XuH-Index: 25
#2Yu JH-Index: 1
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Background: Propofol and sevoflurane are widely used in clinical anesthesia, and both have been reported to exert a protective effect in organ ischemia/reperfusion (IR). This study aims to investigate and compare the effects of propofol and sevoflurane on liver ischemia/reperfusion and the precise molecular mechanism. Methods and Materials: Rats were randomized into four groups: the sham group, I/R group, propofol treatment group (infused with 1% propofol at 500 µg· kg-1· min-1), and sevoflurane...
27 CitationsSource
#1F. WuH-Index: 1
#2X. J. DongH-Index: 1
Last. L. SuH-Index: 1
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Purpose Heat stress stimulation can cause various injuries in human umbilical vein endothelial cells (HUVEC), including apoptotic cell death and an increase in cell permeability. Propofol (PPF), a commonly used anesthetic, is known to have an important role in antioxidation as well as organ protection. Therefore, our aim is to evaluate the protective effects of PPF on heat stress (HS)-induced oxidative stress injury and its possible mechanism of action.
4 CitationsSource
#1Ming Chung Lin (Chung Hwa University of Medical Technology)H-Index: 1
#2Chiou-Feng LinH-Index: 2
Last. Chung-Hsi HsingH-Index: 13
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Prolonged treatment with a large dose of propofol may cause diffuse cellular cytotoxicity; however, the detailed underlying mechanism remains unclear, particularly in vascular endothelial cells. Previous studies showed that a propofol overdose induces endothelial injury and vascular barrier dysfunction. Regarding the important role of endothelial glycocalyx on the maintenance of vascular barrier integrity, we therefore hypothesized that a propofol overdose-induced endothelial barrier dysfunction...
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Propofol, a widely used anesthetic, regulates neurological processes including neurotoxicity, neuroprotection, glial activation, synaptic plasticity and neuronal maturation. Tissue plasminogen activator/tissue plasminogen activator inhibitor-1 (tPA/PAI-1) in CNS acts as a neuromodulator regulating synaptic plasticity, neurite outgrowth, seizure spreading and cell survival. Here, we investigated the effects of propofol on tPA/PAI-1 system using cultured neurons and astrocytes and their role in th...
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#1Dan Pierini (University of Texas Health Science Center at Houston)H-Index: 1
#2Nathan S. Bryan (University of Texas Health Science Center at Houston)H-Index: 38
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#1Ayaz Rahman (Emory University)H-Index: 9
#2Jonathan R. Murrow (Emory University)H-Index: 10
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#2Muharrem UcarH-Index: 12
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We compared postoperative hepatic and renal functions and coagulation profiles in living donors undergoing right hepatectomy under isoflurane (n = 40) versus propofol (n = 40) anesthesia. After induction, anesthesia was maintained with isoflurane/air-O2 (group I) or propofol/air-O2 (group P) in addition to remifentanil and atracurium infusion in both groups. Aspartate aminotransferase, alanine aminotransferase, international normalized ratio (INR), activated partial thromboplastin time (aPTT), a...
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Background Hyperglycemia could induce oxidative stress, activate transcription factor nuclear factor kappa B (NF-κB), up-regulate expression of endothelial adhesion molecules, and lead to endothelial injury. Studies have indicated that propofol could attenuate oxidative stress and suppress NF-κB activation in some situations. In the present study, we examined whether and how propofol improved high glucose-induced up-regulation of endothelial adhesion molecules in human umbilical vein endothelial...
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#2Chein Chi Huang (NCKU: National Cheng Kung University)H-Index: 4
Last. Yen-Chin Liu (NCKU: National Cheng Kung University)H-Index: 19
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Peroxisome proliferator-activated receptor α (PPARα) is involved in the regulation of fatty acid and cholesterol metabolism. A high-cholesterol (HC) diet increases the risk of developing cardiovascular diseases (CVD); however, it is unclear whether the toxic effects of cholesterol involve changes in thrombotic factor expression, and whether PPARα is necessary for such effects. To investigate this possibility, we fed a HC diet to wild-type (WT) and Ppara-null mice and measured cholesterol and tri...
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