title: Emodin improves lipopolysaccharide-induced microcirculatory disturbance in rat mesentery.
abstract: OBJECTIVE
  Sepsis is a systemic inflammatory response syndrome. Emodin is a major ingredient of Rheum Palmatum, a Chinese herb that is widely used in China for treatment of endotoxemia-related diseases. This study intended to examine the effect of Emodin on LPS-induced rat mesenteric microcirculatory disturbance and the underlying mechanisms.
  
  
  METHODS
  The male Wistar rats received LPS (5 mg/kg/hr) for 90 min, with or without administration of Emodin (10 mg/kg/hr) by enema 30 min before (pre-treatment) or after (post-treatment) LPS infusion, and the dynamics of mesenteric microcirculation were determined by inverted intravital microscopy. Expression of adhesion molecules and TLR4, NF-κB p65, ICAM-1, MPO, and AP-1 in mesentery tissue was evaluated by flow cytometry and Western-blot, respectively.
  
  
  RESULTS
  Pre or post-treatment with Emodin significantly ameliorated LPS-induced leukocyte emigration, reactive oxygen species production and albumin leakage, and the expression of TLR4, NF-κB p65, ICAM-1, MPO and AP-1 in mesentery.
  
  
  CONCLUSIONS
  These results demonstrate the beneficial role of Emodin in attenuating the LPS-induced microcirculatory disturbance, and support the use of Emodin for patients with endotoxemia.
authors.affiliation: Department of Critical Care Medicine, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
authors.forename: Ang
authors.initials: A
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Dong
authors.forename: Mei-Li
authors.initials: ML
authors.lastname: Duan
authors.forename: Kai
authors.initials: K
authors.lastname: Sun
authors.forename: Yu-Ying
authors.initials: YY
authors.lastname: Liu
authors.forename: Ming-Xia
authors.initials: MX
authors.lastname: Wang
authors.forename: Jing-Na
authors.initials: JN
authors.lastname: Deng
authors.forename: Jing-Yu
authors.initials: JY
authors.lastname: Fan
authors.forename: Bao-En
authors.initials: BE
authors.lastname: Wang
authors.forename: Jing-Yan
authors.initials: JY
authors.lastname: Han
mesh_terms: D000818:Animals; D004642:Emodin / Q000494:pharmacology*; D019446:Endotoxemia / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D008643:Mesentery / Q000098:blood supply / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008833:Microcirculation / Q000187:drug effects*; D009195:Peroxidase / Q000096:biosynthesis; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000187:drug effects*; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis; D018808:Transcription Factor AP-1 / Q000096:biosynthesis; D051996:Transcription Factor RelA / Q000096:biosynthesis
chemical_list: D008070:Lipopolysaccharides; D047428:Protein Kinase Inhibitors; C498145:Rela protein, rat; C495347:Tlr4 protein, rat; D051197:Toll-Like Receptor 4; D018808:Transcription Factor AP-1; D051996:Transcription Factor RelA; D018799:Intercellular Adhesion Molecule-1; D009195:Peroxidase; D004642:Emodin
keywords: Rheum palmatum; activator protein-1; adhesion molecules; nuclear factor kappa B p65; toll-like receptor 4