RT info:eu-repo/semantics/article
T1 Mechanisms of dexamethasone-mediated chemokine down-regulation in mild and severe acute pancreatitis
A1 Yubero Benito, Sara
A1 Ramudo, Laura
A1 Manso, Manuel Antonio
A1 Dios, Isabel de
K1 Acute pancreatitis
K1 Pancreatitis aguda
K1 Chemokines
K1 Quimiocina
K1 Dexamethasone
K1 Dexametasona
AB 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.
PB Elsevier
SN 0925-4439
YR 2009
FD 2009
LK https://uvadoc.uva.es/handle/10324/46968
UL https://uvadoc.uva.es/handle/10324/46968
LA eng
NO Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2009, vol. 1792, n. 12. p. 1205-1211
NO Producción Científica
DS UVaDOC
RD 16-abr-2024