title: [The mechanism and treatment phases chosen of glycine for inhibition lipopolysaccharide induced Kupffer cells activation].
abstract: OBJECTIVE
  To explore the possible mechanism and optimal treatment phase of glycine for inhibition lipopolysaccharide (LPS) induced Kupffer cells (KCs) activation.
  
  
  METHODS
  The KCs were isolated from 40 BALB/c mice and divided into four groups: the endotoxin group, the prevention group, the early treatment group and the later treatment group (n = 10). The endotoxin group was treated with 10 mg/L LPS, and in the other three groups, glycine (1 mmol/L) was given 24 h before, or at 0 h or 4 h respectively after LPS stimulation. At 0 h, 1 h, 2 h, 6 h and 12 h after LPS stimulation, the mRNA levels and protein expression of interleukin-1 receptor associated kinase-4 (IRAK-4) were determined by reverse transcription polymerase chain reaction (RT-PCR) and Western blot respectively, and nuclear factor-kappaB (NF-kappaB) activities as well as tumor necrosis factor alpha (TNF-alpha) levels were also detected by enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  The climax values of IRAK-4, NF-kappaB and TNF-alpha were significantly higher in the endotoxin group and the later treatment group than that in the other two groups (t = 3.17, 4.33, 2.47, 126.73, P < 0.01).
  
  
  CONCLUSIONS
  The results indicated that prophylactic or simultaneous treatment with glycine could effectively inhibit LPS-induced KCs activation by inhibiting IRAK-4 expression.
authors.affiliation: Department of Hepatobiliary Surgery, the Second Affiliated Hospital of Chongqing University of Medical Sciences, Chongqing 400010, China.
authors.forename: Zuo-jin
authors.initials: ZJ
authors.lastname: Liu
authors.forename: Hai-bo
authors.initials: HB
authors.lastname: You
authors.forename: Xu-hong
authors.initials: XH
authors.lastname: Li
authors.forename: Xian-feng
authors.initials: XF
authors.lastname: Chen
authors.forename: Hai-zhong
authors.initials: HZ
authors.lastname: Liu
authors.forename: Yong
authors.initials: Y
authors.lastname: Peng
authors.forename: Chang-an
authors.initials: CA
authors.lastname: Liu
authors.forename: Jian-ping
authors.initials: JP
authors.lastname: Gong
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D004347:Drug Interactions; D005998:Glycine / Q000008:administration & dosage / Q000494:pharmacology*; D053592:Interleukin-1 Receptor-Associated Kinases; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D007728:Kupffer Cells / Q000187:drug effects* / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D008070:Lipopolysaccharides; D016328:NF-kappa B; D012333:RNA, Messenger; C439524:TNF protein, human; D014409:Tumor Necrosis Factor-alpha; D053592:Interleukin-1 Receptor-Associated Kinases; D017346:Protein Serine-Threonine Kinases; D005998:Glycine