title: Water immersion pretreatment decreases pro-inflammatory cytokine production in cholecystokinin-octapeptide-induced acute pancreatitis in rats: possible role of HSP72.
abstract: Heat shock proteins (HSPs) are cytoprotective proteins that are expressed constitutively and/or at elevated levels upon the exposure of cells to stress. The aim of this study was to investigate the potential effects of HSP preinduction by cold- (CWI) or hot-water immersion (HWI) on pro-inflammatory cytokine production (IL-1, IL-6, TNF-alpha) in cholecystokinin-octapeptide(CCK)-induced acute pancreatitis. Rats were injected with 3 x 75 microg/kg CCK subcutaneously at intervals of 2 h at the peak level of HSP synthesis, as determined by Western blot analysis. The animals were killed by exsanguination through the abdominal aorta 2 h after the last CCK injection. The serum IL-1, IL-6, TNF-alpha, and amylase levels, the pancreatic weight/body weight ratio, and the pancreatic contents of DNA, protein, amylase, lipase and trypsinogen were measured; biopsy for histology was taken. HWI significantly elevated the HSP72 expression, while CWI significantly increased the HSP60 expression. HWI pretreatment decreased all of the measured serum cytokine levels in this acute pancreatitis model. CWI and HWI pretreatment ameliorated most of the examined laboratory and morphological parameters of CCK-induced pancreatitis. The findings suggest the possible roles of HSP60 and HSP72 in the protection against CCK-induced pancreatitis. HSP72 might also participate in the reduction of pro-inflammatory cytokine synthesis.
authors.affiliation: First Department of Medicine, University of Szeged, Hungary. raz@in1st.szote.u-szeged.hu
authors.forename: Z
authors.initials: Z
authors.lastname: Rakonczay
authors.forename: T
authors.initials: T
authors.lastname: Takács
authors.forename: Y
authors.initials: Y
authors.lastname: Mándi
authors.forename: B
authors.initials: B
authors.lastname: Iványi
authors.forename: S
authors.initials: S
authors.lastname: Varga
authors.forename: G
authors.initials: G
authors.lastname: Pápai
authors.forename: I
authors.initials: I
authors.lastname: Boros
authors.forename: J
authors.initials: J
authors.lastname: Lonovics
mesh_terms: D000208:Acute Disease; D000818:Animals; D003080:Cold Temperature; D016207:Cytokines / Q000096:biosynthesis*; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000502:physiology*; D006358:Hot Temperature; D007101:Immersion / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D008854:Microscopy, Electron; D010179:Pancreas / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D010195:Pancreatitis / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology* / Q000517:prevention & control; D051381:Rats; D017208:Rats, Wistar; D012844:Sincalide / Q000633:toxicity
chemical_list: D016207:Cytokines; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D018836:Inflammation Mediators; D012844:Sincalide