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Título
Mechanisms of dexamethasone-mediated chemokine down-regulation in mild and severe acute pancreatitis
Año del Documento
2009
Editorial
Elsevier
Descripción
Producción Científica
Documento Fuente
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2009, vol. 1792, n. 12. p. 1205-1211
Abstract
This study aimed to investigate the role of therapeutic dexamethasone (Dex) treatment on the mechanisms underlying chemokine expression during mild and severe acute pancreatitis (AP) experimentally induced in rats. Regardless of the AP severity, Dex (1 mg/kg), administered 1 h after AP, reduced the acinar cell activation of extracellular signal-regulated kinase (ERK) and c-Jun-NH2-terminal kinase (JNK) but failed to reduce p38-mitogen-activated protein kinase (MAPK) in severe AP. In both AP models, Dex inhibited the activation of nuclear factor-kappaB (NF-κB) and signal transducers and activators of transcription (STAT) factors. All of this resulted in pancreatic down-regulation of the chemokines monocyte chemoattractant protein-1 (MCP-1) and cytokine-induced neutrophil chemoattractant (CINC). Lower plasma chemokine levels as well as decreased amylasemia, hematocrit and plasma interleukin-1β (Il-1β) levels were found either in mild or severe AP treated with Dex. Pancreatic neutrophil infiltration was attenuated by Dex in mild but not in severe AP. In conclusion, by targeting MAPKs, NF-κB and STAT3 pathways, Dex treatment down-regulated the chemokine expression in different cell sources during mild and severe AP, resulting in decreased severity of the disease.
Palabras Clave
Acute pancreatitis
Pancreatitis aguda
Chemokines
Quimiocina
Dexamethasone
Dexametasona
ISSN
0925-4439
Revisión por pares
SI
Patrocinador
Fondo Europeo de Desarrollo Regional - Fondo de Investigación Sanitaria (grant PI08/0035)
Propietario de los Derechos
© 2009 Elsevier
Idioma
eng
Tipo de versión
info:eu-repo/semantics/publishedVersion
Derechos
openAccess
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