Atrial natriuretic peptide reduces inflammation and enhances apoptosis in rat acute pancreatitis
Autor: | Maria Fernanda Rubio, Liliana G. Bianciotti, Marcelo S. Vatta, Juan Carlos Perazzo, Ana Clara Najenson, Ana Paula Courreges |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
medicine.medical_specialty CIENCIAS MÉDICAS Y DE LA SALUD Physiology Apoptosis Caspase 3 Inflammation Fisiología CELL DEATH Secretin Rats Sprague-Dawley 03 medical and health sciences INFLAMMATION Atrial natriuretic peptide Internal medicine medicine Animals Trypsinogen activation TUNEL assay business.industry PANCREATITIS medicine.disease Rats NATRIURETIC PEPTIDES Medicina Básica 030104 developmental biology Endocrinology Pancreatitis Acute pancreatitis Female medicine.symptom business Atrial Natriuretic Factor hormones hormone substitutes and hormone antagonists |
Zdroj: | Acta Physiologica. 222:e12992 |
ISSN: | 1748-1708 |
Popis: | Aim: We previously reported that atrial natriuretic peptide (ANP) reduces serum amylase and intrapancreatic trypsinogen activation in the onset of acute pancreatitis whereas secretin increases them. In the present work, we sought to establish the effect of ANP and secretin on the inflammatory response and cell death in experimental acute pancreatitis. Methods: The expression and activity of key inflammatory mediators and apoptosis were evaluated in the presence or absence of the atrial peptide, secretin or both in cerulein‐induced acute pancreatitis in rats. Also, ultrastructural changes in pancreatic acinar cells were assessed by transmission electron microscopy. Results: ANP significantly reduced NF‐κB activation and TNF‐α intrapancreatic levels. Furthermore, it decreased inducible nitric oxide synthase and cyclooxygenase 2 expression and activity while it diminished myeloperoxidase activity. ANP also stimulated apoptosis as shown by caspase‐3 expression and activation as well as TUNEL assay. These findings correlated well with the ultrastructural changes observed in the exocrine pancreas. Although secretin reduced various inflammatory markers, it also diminished caspase‐3 activation and the overall response was the aggravation of the disease as reflected by the ultrastructural alterations of pancreatic acinar cells. In the presence of ANP, various effects evoked by secretin were antagonized. Conclusion: Present findings show that ANP significantly attenuated the severity of acute pancreatitis in the rat by inducing apoptosis and reducing the inflammatory response and further suggest that ANP may have eventual therapeutic implications in the disease and/or in medical interventions at risk of its developing like endoscopic retrograde cholangiopancreatography. Fil: Najenson, Ana Clara. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Courreges, Ana Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Perazzo, J. C.. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología; Argentina Fil: Rubio, Maria Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina Fil: Vatta, Marcelo Sergio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Metabolismo del Fármaco. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Metabolismo del Fármaco; Argentina Fil: Bianciotti, Liliana Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina |
Databáze: | OpenAIRE |
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