title: Hydroxyethyl starch inhibits intestinal production of cytokines and activation of transcription factors in endotoxaemic rats.
abstract: 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.
authors.affiliation: Department of Anaesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
authors.forename: R
authors.initials: R
authors.lastname: Lv
authors.forename: W
authors.initials: W
authors.lastname: Zhou
authors.forename: J J
authors.initials: JJ
authors.lastname: Yang
authors.forename: Y
authors.initials: Y
authors.lastname: Jin
authors.forename: J G
authors.initials: JG
authors.lastname: Xu
mesh_terms: 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
chemical_list: 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