Hydroxyethyl starch inhibits intestinal production of cytokines and activation of transcription factors in endotoxaemic rats.
We studied the effect of hydroxyethyl starch (HES) on intestinal production of cytokines and activation of transcription factors in sepsis. Septic rats, induced by intraperitoneal lipopolysaccharide (LPS) (5 mg/kg), were treated with intravenous HES (16 ml/kg) or saline (64 ml/kg). Rat ileal tissues were collected at 2 h, 3 h or 6 h after LPS challenge. Levels of tumour necrosis factor alpha (TNF-alpha), interleukin (IL) 1beta, IL-6, IL-8 and IL-10, cytokine mRNAs, activities of nuclear factor kappa-B (NF-KB) and activator protein-1 (AP-1), and the number of ileal myeloperoxidase (MPO)-positive cells were determined for each group. HES significantly reduced the LPS-induced increase in intestinal levels of TNF-alpha, IL-1beta, IL-6, IL-8 and their corresponding mRNAs. HES also decreased the number of MPO-positive cells induced by LPS and inhibited activation of NF-kappaB and AP-1. The results suggest that in sepsis, HES may down-regulate intestinal pro-inflammatory cytokine production via suppression of NF-kappaB and AP-1 activation.
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Department of Anaesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Zhou
W
W
Yang
J J
JJ
Jin
Y
Y
Xu
J G
JG
D000818:Animals; D016207:Cytokines / Q000096:biosynthesis* / Q000378:metabolism; D017931:DNA Primers / Q000737:chemistry; D018076:DNA, Complementary / Q000378:metabolism; D015536:Down-Regulation; D019446:Endotoxemia / Q000628:therapy*; D006895:Hydroxyethyl Starch Derivatives / Q000494:pharmacology*; D007082:Ileum / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D007375:Interleukin-1 / Q000096:biosynthesis; D016753:Interleukin-10 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D016209:Interleukin-8 / Q000096:biosynthesis; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000187:drug effects*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D010952:Plasma Substitutes / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000628:therapy*; D013997:Time Factors; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D016207:Cytokines; D017931:DNA Primers; D018076:DNA, Complementary; D006895:Hydroxyethyl Starch Derivatives; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010952:Plasma Substitutes; D012333:RNA, Messenger; D018808:Transcription Factor AP-1; D014157:Transcription Factors; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D009195:Peroxidase