[HTML][HTML] Relaxin prevents the development of severe acute pancreatitis
LI Cosen-Binker, MG Binker, R Cosen… - World journal of …, 2006 - ncbi.nlm.nih.gov
LI Cosen-Binker, MG Binker, R Cosen, G Negri, O Tiscornia
World journal of gastroenterology: WJG, 2006•ncbi.nlm.nih.govAIM: To investigate the severity of acute pancreatitis (AP) is associated to the intensity of
leukocyte activation, inflammatory up-regulation and microcirculatory disruption associated
to ischemia-reperfusion injury. Microvascular integrity and inhibition of pro-inflammatory
mediators are key-factors in the evolution of AP. Relaxin is an insulin-like hormone that has
been attributed vasorelaxant properties via the nitric oxide pathway while behaving as a
glucocorticoid receptor agonist. METHODS: AP was induced by the bilio-pancreatic duct …
leukocyte activation, inflammatory up-regulation and microcirculatory disruption associated
to ischemia-reperfusion injury. Microvascular integrity and inhibition of pro-inflammatory
mediators are key-factors in the evolution of AP. Relaxin is an insulin-like hormone that has
been attributed vasorelaxant properties via the nitric oxide pathway while behaving as a
glucocorticoid receptor agonist. METHODS: AP was induced by the bilio-pancreatic duct …
Abstract
AIM: To investigate the severity of acute pancreatitis (AP) is associated to the intensity of leukocyte activation, inflammatory up-regulation and microcirculatory disruption associated to ischemia-reperfusion injury. Microvascular integrity and inhibition of pro-inflammatory mediators are key-factors in the evolution of AP. Relaxin is an insulin-like hormone that has been attributed vasorelaxant properties via the nitric oxide pathway while behaving as a glucocorticoid receptor agonist.
METHODS: AP was induced by the bilio-pancreatic duct-outlet-exclusion closed-duodenal-loops model. Treatment with relaxin was done at different time-points. Nitric oxide synthase inhibition by L-NAME and glucocorticoid receptor (GR) blockage by mifepristone was considered. AP severity was assessed by biochemical and histopathological analyses.
RESULTS: Treatment with relaxin reduced serum amylase, lipase, C-reactive protein, IL-6, IL-10, hsp72, LDH and 8-isoprostane as well as pancreatic and lung myeloperoxidase. Acinar and fat necrosis, hemorrhage and neutrophil infiltrate were also decreased. ATP depletion and ADP/ATP ratio were reduced while caspases 2-3-8 and 9 activities were increased. L-NAME and mifepristone decreased the efficiency of relaxin.
CONCLUSION: Relaxin resulted beneficial in the treatment of AP combining the properties of a GR agonist while preserving the microcirculation and favoring apoptosis over necrosis.
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