title: [Primary investigation of the relationship between glucocorticoid induced leucine zipper and inflammatory reaction].
abstract: OBJECTIVE
  To investigate the mechanism of the action of glucocorticoid induced leucine zipper (GILZ) in inflammatory reaction.
  
  
  METHODS
  Human monocyte cell line THP-1 cells were divided into two groups and cultured in non-serum RPMI1640 medium.In one group the cells were treated with dexamethasone (DEX). Twelve hours later total RNA and total protein were abstracted in both two groups. The mRNA encoding for expression of GILZ was semiquantitatively detected by reserve transcriptase-polymerase chain reaction (RT-PCR). Protein expression of nuclear factor-KappaB (NF-KappaB) p65 and activator protein-1 (AP-1) were assessed by Western blotting. Peripheral blood of 10 trauma patients [injury severity score (ISS) >or=16 scores] were collected and the leukocytes were isolated within 24 hours after trauma. The leukocytes were divided into two groups and cultured in non-serum medium. In one group the cells were treated with DEX. Twelve hours later total RNA and total protein were abstracted in both two groups. The mRNA encoding for expression of GILZ was semiquantitatively detected by RT-PCR. Protein expression of NF-KappaB p65 and AP-1 were assessed by Western blotting.
  
  
  RESULTS
  Stimulated by DEX, the expression of GILZ mRNA was increased both in THP-1 cells and the leukocytes of trauma patients compared with those of control groups (both P<0.01). Whereas, protein expressions of NF-KappaB p65 and AP-1 of THP-1 cells and leukocytes in peripheral blood of trauma patients were decreased in the stimulation groups compared with those of control groups (all P<0.01).
  
  
  CONCLUSIONS
  The expression of GILZ gene is up-regulated by glucocorticoid. Overexpression of GILZ inhibits NF-KappaB and AP-1 activities, suggesting that GILZ possesses anti-inflammatory function.
authors.affiliation: Department of Trauma Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China.
authors.forename: Xiang-jun
authors.initials: XJ
authors.lastname: Bai
authors.forename: Bo
authors.initials: B
authors.lastname: Li
authors.forename: Hai-ping
authors.initials: HP
authors.lastname: Wang
authors.forename: Zhao-hui
authors.initials: ZH
authors.lastname: Yang
authors.forename: Si-qi
authors.initials: SQ
authors.lastname: Li
mesh_terms: D000328:Adult; D002460:Cell Line; D003907:Dexamethasone / Q000494:pharmacology*; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000378:metabolism*; D016350:Leucine Zippers / Q000235:genetics / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000378:metabolism; D018808:Transcription Factor AP-1 / Q000378:metabolism; D051996:Transcription Factor RelA / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism*
chemical_list: D005938:Glucocorticoids; D012333:RNA, Messenger; C404226:TSC22D3 protein, human; D018808:Transcription Factor AP-1; D051996:Transcription Factor RelA; D014157:Transcription Factors; D003907:Dexamethasone