PMID- 22453841 OWN - NLM STAT- MEDLINE DCOM- 20121016 LR - 20211021 IS - 1420-908X (Electronic) IS - 1023-3830 (Linking) VI - 61 IP - 7 DP - 2012 Jul TI - Evaluation of N-acetylcysteine treatment in acute pancreatitis-induced lung injury. PG - 699-705 LID - 10.1007/s00011-012-0462-6 [doi] AB - OBJECTIVE: Pulmonary complications are frequent during acute pancreatitis (AP). We investigate the effects of N-acetylcysteine (NAC) on lung injury in mild and severe AP. ANIMALS AND TREATMENT: Mild and severe AP was induced in rats by bile-pancreatic duct obstruction (BPDO) and infusion of 3.5 % sodium taurocholate (NaTc) into the bile-pancreatic duct, respectively. NAC (50 mg/kg) was given 1 h before and 1 h after AP. METHODS: Amylase activity was measured in plasma. Lungs were harvested for mRNA expression analysis of monocyte chemoattractant protein-1 (MCP-1), cytokine-induced neutrophil chemoattractant (CINC), P-selectin and intercellular adhesion molecule-1 (ICAM-1), myeloperoxidase (MPO) activity and histological examination. RESULTS: Hyperamylasemia was reduced by NAC in both AP models. NAC down-regulated MCP-1, CINC and P-selectin in BPDO- but not in NaTc-induced AP. Pulmonary insults did not vary in mild AP and were exacerbated in severe AP by NAC treatment. NAC reduced lung MPO activity in mild but not in severe AP. CONCLUSIONS: Although NAC treatment down-regulated inflammatory mediators in lungs during AP it did not prevent leukocyte infiltration, which could be responsible for maintaining the lung injury. As a result, NAC aggravated the lung damage in severe AP and failed to exert beneficial effects in the mild disease model. FAU - Yubero, Sara AU - Yubero S AD - Departamento Fisiologia y Farmacologia-IBSAL, University of Salamanca, Edificio Departamental, Campus Miguel de Unamuno, 37007 Salamanca, Spain. FAU - Ramudo, Laura AU - Ramudo L FAU - Manso, Manuel A AU - Manso MA FAU - Collia, Francisco AU - Collia F FAU - De Dios, Isabel AU - De Dios I LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20120323 PL - Switzerland TA - Inflamm Res JT - Inflammation research : official journal of the European Histamine Research Society ... [et al.] JID - 9508160 RN - 0 (Ccl2 protein, rat) RN - 0 (Chemokine CCL2) RN - 0 (Chemokine CXCL1) RN - 0 (Cxcl1 protein, rat) RN - 0 (Free Radical Scavengers) RN - 0 (RNA, Messenger) RN - 5E090O0G3Z (Taurocholic Acid) RN - EC 1.11.1.7 (Peroxidase) RN - EC 3.2.1.- (Amylases) RN - WYQ7N0BPYC (Acetylcysteine) SB - IM MH - Acetylcysteine/*therapeutic use MH - Amylases/blood MH - Animals MH - Chemokine CCL2/genetics MH - Chemokine CXCL1/genetics MH - Disease Models, Animal MH - Free Radical Scavengers/*therapeutic use MH - Lung/metabolism/pathology MH - Lung Injury/*drug therapy/etiology/metabolism/pathology MH - Male MH - Pancreatitis/chemically induced/*complications/metabolism/pathology MH - Peroxidase/metabolism MH - RNA, Messenger/metabolism MH - Rats MH - Rats, Wistar MH - Taurocholic Acid EDAT- 2012/03/29 06:00 MHDA- 2012/10/17 06:00 CRDT- 2012/03/29 06:00 PHST- 2012/01/10 00:00 [received] PHST- 2012/03/07 00:00 [accepted] PHST- 2012/02/08 00:00 [revised] PHST- 2012/03/29 06:00 [entrez] PHST- 2012/03/29 06:00 [pubmed] PHST- 2012/10/17 06:00 [medline] AID - 10.1007/s00011-012-0462-6 [doi] PST - ppublish SO - Inflamm Res. 2012 Jul;61(7):699-705. doi: 10.1007/s00011-012-0462-6. Epub 2012 Mar 23.