title: [Effects and mechanisms of cholecystokinin octapeptide on hippocampal injury during endotoxic shock].
abstract: OBJECTIVE
  To study the effects and the mechanisms of cholecystokinin octapeptide(CCK-8) on hippocampal injury during endotoxic shock (ES).
  
  
  METHODS
  Rabbits were injected intravenously with lipopolysaccharide (LPS, 8 mg/kg) to establish ES model. Thirty-two Rabbits were divided into 4 groups at random (n = 8): control (saline, iv), LPS, CCK-8 + LPS (CCK-8 pre-administrated 30 min before LPS, iv), proglumide (Pro, nonspecific antagonist of CCK receptors) + LPS (Pro pre-administrated 30 min before LPS, iv) group. The changes of mean arterial pressure (MAP) were measured. The morphologic changes in the hippocampus were observed through light microscope (LM) and transmission electron microscope (TEM). The alterations of activities of nitric oxide synthase (NOS) and superoxide dismutase (SOD), contents of nitric oxide (NO) and malondialdehyde (MDA) in the hippocampus were assayed. Twelve Sprague-Dawley rats, grouped as that of the rabbits, were used to detect the expression of inducible NOS (iNOS) and neuronal NOS (nNOS) protein by immunohistochemistry staining.
  
  
  RESULTS
  LPS administration resulted insignificant reduction in MAP (P < 0.01 vs control group) and hydropic degeneration of neurons in the hippocampus. Compared with those of control group, the NOS activity, NO level and MDA content were increased significantly (P < 0.05, P < 0.01 and P < 0.05), while SOD activity was reduced (P < 0.01) in the hippocampus of ES rabbits. LPS administration induced the expression of iNOS protein in the cytoplasm of hippocampus neurons, and lead to stronger positive signals of nNOS than that of control group. CCK-8 pre-administration could alleviate the changes induced by LPS, while Pro pre-administration aggravated those alterations.
  
  
  CONCLUSIONS
  CCK-8 could protect hippocampus neurons against the injury induced by LPS during ES, which might be associated with its effects of suppressing the over production of NO and free radicals.
authors.affiliation: Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Wei
authors.forename: Yi-Ling
authors.initials: YL
authors.lastname: Ling
authors.forename: Zhi-Yun
authors.initials: ZY
authors.lastname: Niu
authors.forename: Guo-Chen
authors.initials: GC
authors.lastname: Duan
authors.forename: Shi-Fang
authors.initials: SF
authors.lastname: Yang
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006624:Hippocampus / Q000378:metabolism*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D011817:Rabbits; D051381:Rats; D017207:Rats, Sprague-Dawley; D012772:Shock, Septic / Q000378:metabolism*; D015398:Signal Transduction; D012844:Sincalide / Q000031:analogs & derivatives* / Q000494:pharmacology
chemical_list: C090019:8-sulfocholecystokinin octapeptide; D009569:Nitric Oxide; D012844:Sincalide