Carbon monoxide‐releasing molecule‐3 (CORM ‐3) offers protection in an in vitro model of compartment syndrome
| العنوان: | Carbon monoxide‐releasing molecule‐3 ( |
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| المؤلفون: | David Sanders, Aurelia Bihari, Abdel-Rahman Lawendy, Gediminas Cepinskas, Emil H. Schemitsch, Kyukwang Chung |
| المصدر: | Bone and Joint Institute |
| بيانات النشر: | Wiley, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | Programmed cell death, Physiology, microvascular dysfunction, Leukocyte Rolling, Inflammation, 030204 cardiovascular system & hematology, Pharmacology, medicine.disease_cause, Compartment Syndromes, carbon monoxide, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Physiology (medical), Human Umbilical Vein Endothelial Cells, Organometallic Compounds, Medicine and Health Sciences, medicine, Humans, Molecular Biology, reactive oxygen species, chemistry.chemical_classification, Reactive oxygen species, endothelial integrity, Chemistry, Superoxide, Models, Cardiovascular, apoptosis, cytokines, acute limb compartment syndrome, inflammation, Apoptosis, medicine.symptom, Cardiology and Cardiovascular Medicine, CORM-3, 030217 neurology & neurosurgery, Intracellular, Oxidative stress |
| الوصف: | © 2019 John Wiley & Sons Ltd Objective: Limb compartment syndrome (CS), a complication of trauma, results in muscle necrosis and cell death; ischemia and inflammation contribute to microvascular dysfunction and parenchymal injury. Carbon monoxide-releasing molecule-3 (CORM-3) has been shown to protect microvascular perfusion and reduce inflammation in animal models of CS. The purpose of the study was to test the effect of CORM-3 in human in vitro CS model, allowing exploration of the mechanism(s) of CO protection and potential development of pharmacologic treatment. Methods: Confluent human vascular endothelial cells (HUVECs) were stimulated for 6 h with serum isolated from patients with CS. Intracellular oxidative stress (production of reactive oxygen species (ROS)) apoptosis, transendothelial resistance (TEER), polymorphonuclear leukocyte (PMN) activation and transmigration across the monolayer in response to the CS stimulus were assessed. All experiments were performed in the presence of CORM-3 (100 μM) or its inactive form, iCORM-3. Results: CS serum induced a significant increase in ROS, apoptosis and endothelial monolayer breakdown; it also increased PMN superoxide production, leukocyte rolling and adhesion/transmigration. CORM-3 completely prevented CS-induced ROS production, apoptosis, PMN adhesion, rolling and transmigration, while improving monolayer integrity. Conclusion: CORM-3 offers potent anti-oxidant and anti-inflammatory effects, and may have a potential application to patients at risk of developing CS. |
| تدمد: | 1549-8719 1073-9688 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1ca6892fbc6f104df63087609b3c8997Test https://doi.org/10.1111/micc.12577Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....1ca6892fbc6f104df63087609b3c8997 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15498719 10739688 |
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