title: [Anti-inflammatory action of lipid-bound apoA-I cysteine mutants].
abstract: OBJECTIVE
  To determine the anti-inflammatory functions of different cysteine mutants of apolipoprotein A-I recombinant HDLs.
  
  
  METHODS
  The recombinant HDLs (named rHDL52, rHDL107, rHDL173, rHDLwt) were reconstituted by mixing wild types or their mutants with dipalmitoyl phosphatidylcholine. And the in vivo effects on lipopolysaccharide (LPS)-induced endotoxemia were examined in mice. The plasma levels of plasma tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta and IL-6 in by ELISA were tested. And we also set up two control groups: LPS and saline.
  
  
  RESULTS
  The rHDL52 mice had a significant decrease of plasma TNF-alpha and IL-1beta and the protection of lung against acute injury. 24 h post-injection as compared with rHDLwt group [TNF-alpha: (135.28 +/- 12.84) pg/ml, IL-1beta: (82.00 +/- 8.19) pg/ml], the rHDL52 mice exhibited a higher capability of lowering the plasma levels of TNF-alpha and IL-1beta [(39.66 +/- 2.44) pg/ml, (66.83 +/- 6.24) pg/ml, both P < 0.05]. And, as indicated by histological sections of lung tissue, the rHDL52 mice could also lower the infiltration of inflammatory cells in lung.
  
  
  CONCLUSIONS
  rHDL52 has a higher anti-inflammation capability than wild type rHDLwt.
authors.affiliation: Gout Laboratory, Affiliated Hospital, Medical College of Qingdao University, China.
authors.forename: Yun-long
authors.initials: YL
authors.lastname: Wang
authors.forename: Shu-lai
authors.initials: SL
authors.lastname: Lu
authors.forename: Zhao-he
authors.initials: ZH
authors.lastname: Niu
authors.forename: Zhi-min
authors.initials: ZM
authors.lastname: Miao
authors.forename: Xin-de
authors.initials: XD
authors.lastname: Li
authors.forename: Yan-qiu
authors.initials: YQ
authors.lastname: Zhang
authors.forename: Chang-gui
authors.initials: CG
authors.lastname: Li
authors.forename: Bao-sheng
authors.initials: BS
authors.lastname: Chen
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D016632:Apolipoprotein A-I / Q000235:genetics / Q000494:pharmacology*; D003545:Cysteine / Q000235:genetics / Q000494:pharmacology*; D019446:Endotoxemia / Q000097:blood* / Q000473:pathology; D053583:Interleukin-1beta / Q000097:blood; D008070:Lipopolysaccharides; D008168:Lung / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009005:Monosaccharides; D009154:Mutation; D009842:Oligopeptides; D011994:Recombinant Proteins / Q000235:genetics / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000893:Anti-Inflammatory Agents; D016632:Apolipoprotein A-I; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D009005:Monosaccharides; D009842:Oligopeptides; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; C438940:lipid I; D003545:Cysteine