title: [Receptor mechanisms underlying the modulation of lipopolysaccharide-induced nuclear factor-kappaB expression in vascular endothelial cells by cholecystokinin octapeptide].
abstract: OBJECTIVE
  To elucidate the receptor mechanisms underlying the modulation of lipopolysaccharide (LPS)-induced nuclear factor-kappaB (NF-kappaB) expression in human umbilical vein endothelial cell line ECV-304 cells by cholecystokinin octapeptide (CCK-8).
  
  
  METHODS
  Human umbilical vein endothelial cell line ECV-304 cells were stimulated with vehicle, LPS, CCK-8 (10(-9)-10(-7) mol/L), CCK receptor non-specific antagonist proglumide, CCK-A receptor (CCK-AR) specific antagonist CR-1409 or CCK-B receptor (CCK-BR) specific antagonist CR-2945 singularly or in combination. The NF-kappaB p65 protein level was determined by Western blot and immunocytochemistry technique.
  
  
  RESULTS
  LPS resulted in an increase in the up-regulatory expression and nuclear translocation of NF-kappaB p65 protein in ECV-304 compared with vehicle stimulation. CCK-8 obviously inhibited LPS-induced the changes in NF-kappaB p65 protein in a dose-dependent manner. The inhibitory effects of CCK-8 on NF-kappaB p65 protein expression were attenuated by proglumide>CR-2945>CR-1409.
  
  
  CONCLUSIONS
  CCK-AR and CCK-BR are involved in the mediation of CCK-8 inhibitive regulation for LPS-induced NF-kappaB protein expression in ECV-04 cells, whereas the effect of CCK-BR are more than that of CCK-R.
authors.affiliation: Department of Forensic Medicine and Pathophysiology, Shijiazhuang 050017, Hebei, China. gaofeng761226@163.com
authors.forename: Feng
authors.initials: F
authors.lastname: Gao
authors.forename: Zhen-yong
authors.initials: ZY
authors.lastname: Gu
authors.forename: Jing
authors.initials: J
authors.lastname: Ping
authors.forename: Xing-yun
authors.initials: XY
authors.lastname: Wang
authors.forename: Xia
authors.initials: X
authors.lastname: Liu
authors.forename: Jin-rong
authors.initials: JR
authors.lastname: Xu
authors.forename: Li
authors.initials: L
authors.lastname: Zhao
authors.forename: Yu-xian
authors.initials: YX
authors.lastname: Yan
authors.forename: Li-qin
authors.initials: LQ
authors.lastname: Ma
authors.forename: Bin
authors.initials: B
authors.lastname: Cong
authors.forename: Yi-ling
authors.initials: YL
authors.lastname: Ling
mesh_terms: D001569:Benzodiazepines / Q000494:pharmacology; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology; D016328:NF-kappa B / Q000378:metabolism*; D011377:Proglumide / Q000031:analogs & derivatives / Q000494:pharmacology; D043886:Receptor, Cholecystokinin A / Q000037:antagonists & inhibitors / Q000378:metabolism*; D043887:Receptor, Cholecystokinin B / Q000037:antagonists & inhibitors / Q000378:metabolism*; D012844:Sincalide / Q000494:pharmacology*; D014471:Umbilical Veins / Q000166:cytology
chemical_list: C116183:CR 2945; D008070:Lipopolysaccharides; D016328:NF-kappa B; D043886:Receptor, Cholecystokinin A; D043887:Receptor, Cholecystokinin B; D001569:Benzodiazepines; D011377:Proglumide; C048181:lorglumide; D012844:Sincalide