title: Hydroxyethyl starch exhibits antiinflammatory effects in the intestines of endotoxemic rats.
abstract: We performed the present in vivo study to investigate the effect of hydroxyethyl starch (HES) on intestinal production of inflammatory mediators and activation of transcription factors during endotoxemia. Rats with endotoxemia induced by lipopolysaccharide (LPS) (5 mg/kg, IV) were treated with HES (16 mL/kg, IV) or saline (64 mL/kg, IV). At 2, 3, or 6 h after the LPS challenge, the rat ileal tissues were collected. Various ileal inflammatory mediator levels (tumor necrosis factor-alpha, interleukin [IL]-6, cytokine-induced neutrophil chemoattractant-1, and IL-10), inflammatory mediator messenger RNAs (mRNAs), activities of nuclear factor (NF)-kappaB and activator protein (AP)-1, and ileal myeloperoxidase-positive cells were determined in each group. HES significantly reduced the increased intestinal levels of tumor necrosis factor-alpha, IL-6, cytokine-induced neutrophil chemoattractant-1, and the mRNAs in the endotoxemic rats. Similarly, HES could decrease the myeloperoxidase-positive cells induced by LPS and also inhibit ileal NF-kappaB and AP-1 activations. Our results suggest that during endotoxemia HES may down-regulate intestinal inflammatory mediator production, and this antiinflammatory effect of HES may act through suppression of NF-kappaB and AP-1 activations.
authors.affiliation: Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, 305 East Zhongshan Road, Nanjing 210002, PR China. nulvran@yahoo.com.cn
authors.forename: Ran
authors.initials: R
authors.lastname: Lv
authors.forename: Zhi-Qiang
authors.initials: ZQ
authors.lastname: Zhou
authors.forename: Hai-Wei
authors.initials: HW
authors.lastname: Wu
authors.forename: Yi
authors.initials: Y
authors.lastname: Jin
authors.forename: Wei
authors.initials: W
authors.lastname: Zhou
authors.forename: Jian-Guo
authors.initials: JG
authors.lastname: Xu
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D019743:Chemokines, CXC / Q000378:metabolism; D019446:Endotoxemia / Q000378:metabolism*; D004926:Escherichia coli; D006895:Hydroxyethyl Starch Derivatives / Q000494:pharmacology*; D007082:Ileum / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism*; D016753:Interleukin-10 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D051818:Replication Protein C / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D019743:Chemokines, CXC; D006895:Hydroxyethyl Starch Derivatives; D018836:Inflammation Mediators; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D009195:Peroxidase; D051818:Replication Protein C