Preconditioning of Carbon Monoxide Releasing Molecule-derived CO Attenuates LPS-induced Activation of HUVEC
| Autor: | Bing-Wei Sun, Xiang-qian Zou, Yueling Chen, Ping Zhang, Geng-sheng Shi |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
Lipopolysaccharides
Umbilical Veins ICAM-1 Blotting Western Intercellular Adhesion Molecule-1 Nitric Oxide Synthase Type II Electrophoretic Mobility Shift Assay Enzyme-Linked Immunosorbent Assay Nitric Oxide medicine.disease_cause Applied Microbiology and Biotechnology NF-κB Nitric oxide chemistry.chemical_compound Downregulation and upregulation Western blot preconditioning Organometallic Compounds medicine oxidative stress Humans Molecular Biology Cells Cultured Ecology Evolution Behavior and Systematics Carbon Monoxide medicine.diagnostic_test Infant Newborn Endothelial Cells Cell Biology Molecular biology chemistry Heme Oxygenase (Decyclizing) Electrophoresis Polyacrylamide Gel Intracellular Oxidative stress Research Paper Developmental Biology |
| Zdroj: | International Journal of Biological Sciences |
| ISSN: | 1449-2288 |
| DOI: | 10.7150/ijbs.4.270 |
| Popis: | Objective: To investigate the effects and potential mechanisms of preconditioning of tricarbonyldichlororuthenium (III) dimer (CORM-2)-liberated CO on LPS-induced activation of endothelial cells (HUVEC). Methods: HUVEC were pretreated with CORM-2 at the concentration of 50 or 100μM for 2 hrs, washed and stimulated with LPS (10μg/ml) for additional 4 hrs. Activation (oxidative stress) of HUVEC was assessed by measuring intracellular oxidation of DHR 123 or nitration of DAF-FM, specific H2O2 and NO fluorochromes, respectively. The expression of HO-1, iNOS (Western blot) and ICAM-1 (cell ELISA) proteins and activation of inflammation-relevant transcription factor, NF-κB (EMSA) were assessed. In addition, PMN adhesion to HUVEC was also assessed. Results: The obtained data indicate that pretreatment of HUVEC with CORM-2 results in: 1) decrease of LPS-induced production of ROS and NO; 2) up-regulation of HO-1 but decrease in iNOS at the protein levels; 3) inhibition of LPS-induced activation of NF-κB; and 4) downregulation of expression of ICAM-1, and this was accompanied by a decrease of PMN adhesion to LPS-stimulated HUVEC. Conclusions: Preconditioning of CO liberated by CORM-2 elicited its anti-inflammatory effects by interfering with the induction of intracellular oxidative stress. In addition, it also supports the notion that CO is a potent inhibitor of iNOS and NF-κB. |
| Databáze: | OpenAIRE |
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