Hydroxyethyl starch exhibits antiinflammatory effects in the intestines of endotoxemic rats.
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.
Lv
Ran
R
Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, 305 East Zhongshan Road, Nanjing 210002, PR China. nulvran@yahoo.com.cn
Zhou
Zhi-Qiang
ZQ
Wu
Hai-Wei
HW
Jin
Yi
Y
Zhou
Wei
W
Xu
Jian-Guo
JG
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
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