title: p38 MAPK inhibition alleviates experimental acute pancreatitis in mice.
abstract: BACKGROUND
  The mitogen-activated protein kinases (MAPKs) signaling pathway is involved in inflammatory process. However, the mechanism is not clear. The present study was to investigate the role of p38 MAPK in acute pancreatitis in mice.
  
  
  METHODS
  Mice were divided into 4 groups: saline control; acute pancreatitis induced with repeated injections of cerulein; control plus p38 MAPK inhibitor SB203580; and acute pancreatitis plus SB203580. The pancreatic histology, pancreatic enzymes, cytokines, myeloperoxidase activity, p38 MAPK and heat shock protein (HSP) 60 and 70 were evaluated.
  
  
  RESULTS
  Repeated injections of cerulein resulted in acute pancreatitis in mice, accompanying with the activation of p38 MAPK and overexpression of HSP60 and HSP70 in the pancreatic tissues. Treatment with SB203580 significantly inhibited the activation of p38 MAPK, and furthermore, inhibited the expression of HSP60 and HSP70 in the pancreas, the inflammatory cytokines in the serum, and myeloperoxidase activity in the lung.
  
  
  CONCLUSIONS
  The p38 MAPK signaling pathway is involved in the regulation of inflammatory response and the expression of HSP60 and HSP70 in acute pancreatitis.
authors: Department of Pathophysiology, Institute of Digestive Disease, Tongji University School of Medicine, Shanghai 200092, China. liyongyu@tongji.edu.cn.
authors: Ming-Hua
authors: MH
authors: Cao
authors: Jing
authors: J
authors: Xu
authors: Hai-Dong
authors: HD
authors: Cai
authors: Zhong-Wei
authors: ZW
authors: Lv
authors: Ya-Jing
authors: YJ
authors: Feng
authors: Kun
authors: K
authors: Li
authors: Chun-Qiu
authors: CQ
authors: Chen
authors: Yong-Yu
authors: YY
authors: Li
mesh_terms: D000208:Acute Disease; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D015415:Biomarkers / Q000097:blood; D002108:Ceruletide; D018834:Chaperonin 60 / Q000378:metabolism; D004195:Disease Models, Animal; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D007093:Imidazoles / Q000494:pharmacology*; D018836:Inflammation Mediators / Q000097:blood; D008168:Lung / Q000187:drug effects / Q000201:enzymology; D008810:Mice, Inbred C57BL; D024101:Mitochondrial Proteins / Q000378:metabolism; D010179:Pancreas / Q000187:drug effects* / Q000201:enzymology / Q000276:immunology; D010195:Pancreatitis / Q000139:chemically induced / Q000201:enzymology / Q000276:immunology / Q000517:prevention & control; D009195:Peroxidase / Q000378:metabolism; D010766:Phosphorylation; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*; D011725:Pyridines / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D018834:Chaperonin 60; D018840:HSP70 Heat-Shock Proteins; C557066:Hspd1 protein, mouse; D007093:Imidazoles; D018836:Inflammation Mediators; D024101:Mitochondrial Proteins; D047428:Protein Kinase Inhibitors; D011725:Pyridines; D002108:Ceruletide; D009195:Peroxidase; D048051:p38 Mitogen-Activated Protein Kinases; C093642:SB 203580