Effects of glucocorticoid agonist and antagonist on the pathogenesis of L-arginine-induced acute pancreatitis in rat
Objectives: To investigate the consequences of treatment with an exogenous glucocorticoid agonist (methylprednisolone) and antagonist (RU-38486) on the local and systemic responses in L-arginine-induced acute pancreatitis in rats. Methods: The methylprednisolone and RU-38486 were administered just b...
Elmentve itt :
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| Dokumentumtípus: | Cikk |
| Megjelent: |
2008
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| Sorozat: | PANCREAS
36 No. 4 |
| doi: | 10.1097/MPA.0b013e31815bd26a |
| mtmt: | 1401345 |
| Online Access: | http://publicatio.bibl.u-szeged.hu/18778 |
| LEADER | 02621nab a2200289 i 4500 | ||
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| 001 | publ18778 | ||
| 005 | 20200529155142.0 | ||
| 008 | 200529s2008 hu o 0|| zxx d | ||
| 022 | |a 0885-3177 | ||
| 024 | 7 | |a 10.1097/MPA.0b013e31815bd26a |2 doi | |
| 024 | 7 | |a 1401345 |2 mtmt | |
| 040 | |a SZTE Publicatio Repozitórium |b hun | ||
| 041 | |a zxx | ||
| 100 | 1 | |a Paszt Attila | |
| 245 | 1 | 0 | |a Effects of glucocorticoid agonist and antagonist on the pathogenesis of L-arginine-induced acute pancreatitis in rat |h [elektronikus dokumentum] / |c Paszt Attila |
| 260 | |c 2008 | ||
| 300 | |a 369-376 | ||
| 490 | 0 | |a PANCREAS |v 36 No. 4 | |
| 520 | 3 | |a Objectives: To investigate the consequences of treatment with an exogenous glucocorticoid agonist (methylprednisolone) and antagonist (RU-38486) on the local and systemic responses in L-arginine-induced acute pancreatitis in rats. Methods: The methylprednisolone and RU-38486 were administered just before pancreatitis induction. Plasma amylase activity, interleukin 6 activity, pancreatic weight/body weight ratio, plasma macrophage migration inhibitory factor (MIF) concentration, and pancreatic nuclear transcription factor (NF) kappa B activity were determined. The extents of pancreas, liver, and lung injurieswere assessed by histology. Results: Acute pancreatitis resulted in NF-kappa B activation and proinflammatory cytokine release in rats. In the glucocorticoid agonist group, plasma amylase and interleukin 6 levels were significantly decreased as compared with those of RU-38486 and nontreated groups. Antagonist treatment led to significantly higher MIF production at 8 and 12 hours after L-arginine injection as compared with the agonist-treated and nontreated groups. Glucocorticoid agonist treatment significantly decreased the level of NF-kappa B 24 hours after pancreatitis induction. Histological investigations showed protective effect of agonist treatment on acute pancreatitis-induced tissue damage in the pancreas and lung. Conclusions: These results corroborated the importance of MIF in acute pancreatitis. The glucocorticoid- dependent mechanisms seem to play a crucial role in the control of the inflammatory response and tissue damage in L-arginine-induced experimental acute pancreatitis. | |
| 700 | 0 | 2 | |a L. Éder Katalin |e aut |
| 700 | 0 | 2 | |a Szabolcs Annamária |e aut |
| 700 | 0 | 2 | |a Tiszlavicz László |e aut |
| 700 | 0 | 2 | |a Lázár György ifj. |e aut |
| 700 | 0 | 2 | |a Duda Ernő |e aut |
| 700 | 0 | 2 | |a Takács Tamás |e aut |
| 700 | 0 | 2 | |a Lázár György ifj |e aut |
| 856 | 4 | 0 | |u http://publicatio.bibl.u-szeged.hu/18778/1/paszt_effects_pancreas_2008-4_369-76.pdf |z Dokumentum-elérés |