Dietary glycine prevents chemical-induced experimental colitis in the rat.
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.
Tsune
Isao
I
Department of Gastroenteroligy, Jutendo University School of Medicine, Tokyo, Japan.
Ikejima
Kenichi
K
Hirose
Miyoko
M
Yoshikawa
Mutsuko
M
Enomoto
Nobuyuki
N
Takei
Yoshiyuki
Y
Sato
Nobuhiro
N
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
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