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  • Title: Propofol reduces apoptosis and up-regulates endothelial nitric oxide synthase protein expression in hydrogen peroxide-stimulated human umbilical vein endothelial cells.
    Author: Wang B, Luo T, Chen D, Ansley DM.
    Journal: Anesth Analg; 2007 Oct; 105(4):1027-33, table of contents. PubMed ID: 17898383.
    Abstract:
    BACKGROUND: Vascular endothelial cells play an important role in maintaining cardiovascular homeostasis. Oxidative stress is a critical pathogenic factor in endothelial cell damage and the development of cardiovascular diseases. In this study we evaluated the effects of propofol on oxidative stress-induced endothelial cell insults and the role of serine-threonine kinase Akt modulation of endothelial nitric oxide synthase (eNOS) as a mechanism of protection. METHODS: Human umbilical vein endothelial cells were used as the experimental model. Hydrogen peroxide (H2O2, 100 microM) was used as the stimulus of oxidative stress. Study groups included 1) control; 2) cells incubated with H2O2 alone; 3) cells incubated with propofol (50 microM) alone; or 4) cells pretreated with propofol 50 microM for 30 min then co-incubated with H2O2. Cell viability was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and Trypan blue dye exclusion test. Cell apoptosis was evaluated by Hoechst 33258 staining. Caspase-3 activity was determined by the colorimetric CaspACE Assay System. Expressions of Akt, phospho-Akt, and eNOS were detected by Western blotting. RESULTS: H2O2 decreased cell viability, induced apoptosis, and increased caspase-3 activity in human umbilical vein endothelial cells. Propofol significantly protected cells from H2O2-induced cell damage, apoptosis and decreased H2O2-induced increase in caspase-3 activity. Propofol treatment significantly increased eNOS expression compared to control and H2O2-stimulated cells. There was no significant difference in phospho-Akt (Ser 473 or Thr 308) expression among the groups. CONCLUSIONS: Propofol 50 microM can reduce H2O2-induced damage and apoptosis in endothelial cells, by suppressing caspase-3 activity and by increasing eNOS expression via an Akt-independent mechanism.
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