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Publication
Hydroxyproline Attenuates Dextran Sulfate Sodium-Induced Colitis in Mice:
Involvment of the NF-?B Signaling and Oxidative Stress.
Authors Ji Y, Dai Z, Sun S, Ma X, Yang Y, Tso P, Wu G, Wu Z
Submitted By Submitted Externally on 2/22/2019
Status Published
Journal Molecular nutrition & food research
Year 2018
Date Published 11/1/2018
Volume : Pages 62 : e1800494
PubMed Reference 30184329
Abstract Inflammatory bowel disease (IBD) is a chronic disease of gastrointestinal tract
in which oxidative stress and overactivation of inflammatory response are
implicated. The aim of the present study is to test the hypothesis that
hydroxyproline (Hyp), an amino acid with an antioxidative property, attenuates
dextran sulfate sodium (DSS)-induced colitis in mice., Male C57BL/6 mice
supplemented with or without 1% Hyp are subjected to 2.5% DSS in drinking water
to induce colitis. Hyp attenuates the severity of colitis as evidenced by
reduced disease activity index scores, decreased myeloperoxidase activity,
histological damage, and apoptosis. Furthermore, DSS-induced increases in
reactive oxygen species accumulation, TNF-a and IL-6 secretion, and
malonyldialdehyde activity and a decrease in reduced glutathione in the colon
are ameliorated by Hyp. The enhanced phosphorylation of STAT3 and NF-?B
following DSS administration is mitigated by Hyp, which is also observed in
LPS-treated RAW264.7 macrophages. Moreover, the inhibitory effect of Hyp on IL-6
expression is mainly mediated by the NF-?B signaling, because the induction of
STAT3 and IL-6 by LPS is markedly reversed by Bay11-7085, a specific inhibitor
NF-?B., In summary, Hyp is a critical nutrient with an ability to attenuate
DSS-induced colonic damage in mice. This beneficial effect of Hyp is partially
mediated by inhibiting the NF-?B/IL-6 signaling and the restoration of redox
homeostasis.




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