title: Honokiol rescues sepsis-associated acute lung injury and lethality via the inhibition of oxidative stress and inflammation.
abstract: OBJECTIVE
  Sepsis has a high mortality rate despite the recent advances in intensive care medicine and antibiotics. Honokiol, a low molecular weight natural product, is known to possess anti-inflammatory activity. Here, we investigate whether honokiol can ameliorate acute lung injury and lethal response in murine models of sepsis.
  
  
  METHODS
  Mice were intraperitoneally given vehicle or honokiol 30 min after the induction of sepsis by cecal ligation and puncture (CLP) and endotoxemia by administration of E. coli lipopolysaccharide (LPS).
  
  
  RESULTS
  The productions of serum tumor necrosis factor-α (TNF-α), nitric oxide (NO), and high mobility group box 1 (HMGB 1) were increased in mice during sepsis, which could be reversed by honokiol. Honokiol could also effectively reduce the increased blood lipid peroxidation and nitrotyrosine in septic mice. Honokiol significantly reversed the inductions of inducible NO synthase and nuclear factor-κB (NF-κB) activation in the lungs of mice during sepsis. Honokiol also effectively rescued the lung edema, lung pathological changes, and lethality in septic mice.
  
  
  CONCLUSIONS
  These findings suggest that honokiol is capable of suppressing the lethal response and acute lung injury associated with sepsis, and support the potential use of honokiol as a therapeutic agent for the conditions associated with septic shock.
authors.affiliation: Department of Forensic Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan. wengtei2@ntu.edu.tw
authors.forename: Te I
authors.initials: TI
authors.lastname: Weng
authors.forename: Hsiao Yi
authors.initials: HY
authors.lastname: Wu
authors.forename: Chia Wei
authors.initials: CW
authors.lastname: Kuo
authors.forename: Shing Hwa
authors.initials: SH
authors.lastname: Liu
mesh_terms: D055371:Acute Lung Injury / Q000188:drug therapy* / Q000209:etiology* / Q000276:immunology / Q000401:mortality / Q000503:physiopathology; D000818:Animals; D000890:Anti-Infective Agents / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D001713:Biphenyl Compounds / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D019446:Endotoxemia / Q000209:etiology; D007249:Inflammation / Q000517:prevention & control*; D017705:Lignans / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000633:toxicity; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D018384:Oxidative Stress / Q000187:drug effects*; D018805:Sepsis / Q000150:complications*; D000498:Allyl Compounds; D010636:Phenols
chemical_list: D000890:Anti-Infective Agents; D001713:Biphenyl Compounds; D017705:Lignans; D008070:Lipopolysaccharides; C433788:lipopolysaccharide, E. coli O26-B6; C005499:honokiol; D000498:Allyl Compounds; D010636:Phenols