RESUMEN
Apolipoprotein M (ApoM) is a type of apolipoprotein. It is well known that highdensity lipoprotein (HDL) decreases inflammatory responses via the apoMsphingosine1phosphate (S1P) pathway. The present study further investigated the importance of ApoM in the inhibitory effects of HDL on inflammation. Mice with an apoM gene deficiency (apoM/) were employed to investigate the effects of ApoM on the expression of interleukin1ß (IL1ß), monocyte chemotactic protein1 (MCP1), S1P receptor1 (S1PR1) and 3ßhydroxysterol Δ24reductase (DHCR24), as compared with in wildtype mice (apoM+/+). Furthermore, cell culture experiments were performed using a permanent human hybrid endothelial cell line (EA.hy926). Cells were cultured in the presence of recombinant human apoM (recapoM) or were induced to overexpress apoM (apoMTg); subsequently, cells were treated with tumor necrosis factorα (TNFα), in order to investigate the effects of ApoM on IL1ß and MCP1. The results demonstrated that the mRNA expression levels of IL1ß and MCP1 were significantly higher in the liver following administration of lipopolysaccharide in apoM/ mice compared with in apoM+/+ mice. In cell culture experiments, when cells were precultured with recapoM or were engineered to overexpress apoM (apoMTg), they exhibited decreased expression levels of IL1ß and MCP1 following TNFα treatment compared with in normal apoMexpressing cells (apoMTgN). Furthermore, the mRNA expression levels of IL1ß and MCP1 were significantly elevated following addition of the S1PR1 inhibitor W146, but not by the scavenger receptor class B type I inhibitor, block lipid transport1 (BLT1), in apoMTg cells prior to TNFα treatment. Conversely, there were no differences in these inflammatory biomarkers under the same conditions in apoMTgN cells. The mRNA expression levels of DHCR24 were significantly reduced by the addition of BLT1 prior to TNFα treatment in apoMTg cells; however, there was no difference in the expression of this inflammatory biomarker in apoMTgN cells. In conclusion, ApoM displayed inhibitory effects against the inflammatory response in vivo and in vitro; these effects may be induced via the S1PR1 and DHCR24 pathways.
Asunto(s)
Apolipoproteínas M/metabolismo , Inflamación/metabolismo , Proteínas del Tejido Nervioso/metabolismo , Oxidorreductasas actuantes sobre Donantes de Grupo CH-CH/metabolismo , Receptores de Lisoesfingolípidos/metabolismo , Transducción de Señal/fisiología , Animales , Biomarcadores/metabolismo , Línea Celular , Quimiocina CCL2/metabolismo , Humanos , Lipoproteínas HDL/metabolismo , Hígado/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , ARN Mensajero/metabolismo , Receptores de Esfingosina-1-Fosfato , Factor de Necrosis Tumoral alfa/metabolismoRESUMEN
According to the literature, only a small proportion of occurrences regarding penetrating trauma of the thoracic aorta can be treated successfully. Herein we reported our experience of a recent rescue of such a patient in a countryside hospital lacking advanced instruments for cardiopulmonary bypass operations. A 20-year-old male was admitted for a penetrating injury with disrupted innominate vein and right common carotid artery together with a 1.5-cm laceration on the aortic arch between the innominate artery and the left common carotid artery. The patient was successfully saved without the implementation of cardiopulmonary bypass. Presentation and management in this case were discussed.
Asunto(s)
Aorta Torácica/lesiones , Heridas Penetrantes/cirugía , Adulto , Aorta Torácica/cirugía , Humanos , MasculinoRESUMEN
OBJECTIVE: To discuss our experience on the diagnosis and treatment of thoracic aorta rupture (TAR) that is one of the main common causes of death in the victims under blunt chest trauma. METHODS: Between July 2001 and March 2006, 9 patients (6 men and 3 women, aged from 20 to 54 years) suffering from acute traumatic aorta rupture after motor vehicle accidents received emergent surgical treatments in our hospital. Based on our experience in the rescue of the first TAR patient we introduced a practical procedure on the diagnosis and treatment of TAR in our department. All the other patients generally followed this procedure. Eight patients received contrast material enhanced helical computerized tomography scan before the operation. The leakage of constrast medium from the aorta isthmus was found, and diagnosis of TAR was confirmed. Seven patients underwent immediate operation within 14 hours after accidents. One patient was treated on the 5th day of the accident because of delayed diagnosis of aortic rupture. All patients received general anesthesia with double lumen endotracheal tube and normothermic femoro-femoral partial cardiopulmonary bypass, with beating heart and aortic clamping. One patient received simple repair, and others received partial replacement of thoracic aorta with artificial vascular graft. RESULTS: Seven TAR patients were successfully salvaged. Three patients combined brain injury as well as extremitiy hemiplegia before operation. After treatments one was fully and two partially recovered without paraplegia. CONCLUSIONS: Proper practical protocol is emphasized for the surgical repair of TAR because it will reduce the mortality of severe blunt chest injury.