title: Effect of cholecystokinin on cytokines during endotoxic shock in rats.
abstract: OBJECTIVE
  To study the effect of cholecystokinin-octapeptide (CCK-8) on systemic hypotension and cytokine production in lipopolysaccharide (LPS)-induced endotoxic shock (ES) rats.
  
  
  METHODS
  The changes of blood pressure were observed using physiological record instrument in four groups of rats: LPS (8mg.kg(-1),iv) induced ES; CCK-8 (40 microg.kg(-1), iv) pretreatment 10 min before LPS (8mg.kg(-1)); CCK-8 (40 micro.kg(-1), iv) or normal saline (control) groups. Differences in tissue and circulating specificity of the proinflammatory cytokines (TNF-alpha, IL-1beta and IL-6) were assayed with ELISA kits.
  
  
  RESULTS
  CCK-8 reversed LPS-induced decrease of mean artery blood pressure (MABP) in rats. Compared with control, LPS elevated the serum level of IL-6 significantly (3567 +/- 687 ng.L(-1) vs 128 +/- 22 ng.L(-1), P<0.01), while contents of TNF-alpha and IL-1beta elevated significantly (277 +/- 86 ng.L(-1) vs not detectable and 43 +/- 9 ng.L(-1) vsnot detectable, P<0.01) but less extent than IL-6. CCK-8 significantly inhibited the LPS-induced increase in serum TNF-alpha IL-1beta and IL-6. LPS elevated spleen and lung content of IL-1beta significantly (5184 +/- 85 ng.L(-1) vs 1047 +/- 21 ng.L(-1) and 4050 +/- 614 ng.L(-1) vs not detectable, P<0.01), while levels of TNF-alpha and IL-6 also rose significantly but in less extent than IL-1beta. CCK-8 inhibited the LPS-induced increase of the cytokines in spleen and lung. In the heart, CCK-8 significantly inhibited LPS-induced increase of TNF-alpha (864 +/- 123 ng.L(-1) in CCK-8+LPS group vs 1599 +/- 227 ng.L(-1) in LPS group, P < 0.01), and IL-1beta (282 +/- 93 ng.L(-1) in CCK-8+LPS group vs 621 +/- 145ng.L(-1) in LPS group, P < 0.01).
  
  
  CONCLUSIONS
  CCK-8 reverses ES, which may be related to its inhibitory effect on the overproduction of cytokines.
authors.affiliation: Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, Hebei Province, China. LingYL20@sina.com.cn
authors.forename: Y L
authors.initials: YL
authors.lastname: Ling
authors.forename: A H
authors.initials: AH
authors.lastname: Meng
authors.forename: X Y
authors.initials: XY
authors.lastname: Zhao
authors.forename: B E
authors.initials: BE
authors.lastname: Shan
authors.forename: J L
authors.initials: JL
authors.lastname: Zhang
authors.forename: X P
authors.initials: XP
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D016207:Cytokines / Q000096:biosynthesis* / Q000097:blood; D007375:Interleukin-1 / Q000096:biosynthesis / Q000097:blood; D015850:Interleukin-6 / Q000096:biosynthesis / Q000097:blood; D008070:Lipopolysaccharides; D008168:Lung / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012772:Shock, Septic / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism*; D012844:Sincalide / Q000494:pharmacology*; D013047:Specific Pathogen-Free Organisms; D013154:Spleen / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000378:metabolism
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D012844:Sincalide