title: Dietary glycine prevents chemical-induced experimental colitis in the rat.
abstract: OBJECTIVE
  In this study, the effect of dietary glycine on experimental colitis induced by 2,4,6-trinitrobenzene sulphonic acid (TNBS) and dextran sulfate sodium (DSS) in the rat was evaluated.
  
  
  METHODS
  Male Wistar rats were fed a diet containing 5% glycine or casein as controls starting 3 days before experiments, and were given a single intracolonic injection of TNBS (50 mg/rat, dissolved in 50% ethanol). Similarly, some rats were given 3% DSS orally in drinking water for 5 days to induce colitis as a second model. The severity of colitis was evaluated pathologically, and tissue myeloperoxidase (MPO) activity was measured. Further, mRNA and protein levels for interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, cytokine-induced neutrophil chemoattractant (CINC), and macrophage inflammatory protein (MIP)-2 were detected by reverse-transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively.
  
  
  RESULTS
  A diet containing glycine ameliorated diarrhea and body weight loss caused by TNBS, and improved both macroscopic and histologic scores of colitis significantly. TNBS-induced increases in MPO activities in the colonic tissue were blunted significantly in glycine-fed animals. Further, dietary glycine largely prevented increases in IL-1beta and TNF-alpha in the colon 2 days after TNBS, and TNBS induction of CINC and MIP-2 in the colonic tissue also was abrogated by glycine. Importantly, the protective effect of glycine was significant even when TNBS colitis was once established. Moreover, dietary glycine also was preventive in a second, DSS-induced colitis model.
  
  
  CONCLUSIONS
  Dietary glycine prevents chemical-induced colitis by inhibiting induction of inflammatory cytokines and chemokines. It is postulated that glycine may be useful for the treatment of inflammatory bowel diseases as an immunomodulating nutrient.
authors.affiliation: Department of Gastroenteroligy, Jutendo University School of Medicine, Tokyo, Japan.
authors.forename: Isao
authors.initials: I
authors.lastname: Tsune
authors.forename: Kenichi
authors.initials: K
authors.lastname: Ikejima
authors.forename: Miyoko
authors.initials: M
authors.lastname: Hirose
authors.forename: Mutsuko
authors.initials: M
authors.lastname: Yoshikawa
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Enomoto
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Takei
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Sato
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D054426:Chemokine CXCL2; D018925:Chemokines / Q000235:genetics; D019743:Chemokines, CXC; D003092:Colitis / Q000139:chemically induced / Q000517:prevention & control*; D003106:Colon / Q000201:enzymology; D016207:Cytokines / Q000235:genetics; D005998:Glycine / Q000008:administration & dosage*; D036341:Intercellular Signaling Peptides and Proteins; D007375:Interleukin-1 / Q000235:genetics; D008297:Male; D015846:Monokines / Q000235:genetics; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014302:Trinitrobenzenesulfonic Acid / Q000633:toxicity; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D054426:Chemokine CXCL2; D018925:Chemokines; D019743:Chemokines, CXC; C513296:Cxcl2 protein, rat; D016207:Cytokines; D036341:Intercellular Signaling Peptides and Proteins; D007375:Interleukin-1; D015846:Monokines; D014409:Tumor Necrosis Factor-alpha; D014302:Trinitrobenzenesulfonic Acid; D009195:Peroxidase; D005998:Glycine