Egg yolk phosphatidylcholine alleviates DSS-induced colitis in BALB/c mice
Ulcerative colitis (UC) is a common inflammatory bowel disease, whose incidence is on the rise worldwide. The drugs commonly used for UC are often associated with a number of side effects. Therefore, the development of effective, food-borne substances for UC is in line with the current needs. Egg yo...
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Published in | Food & function Vol. 14; no. 2; pp. 939 - 9323 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Cambridge
Royal Society of Chemistry
16.10.2023
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Subjects | |
Online Access | Get full text |
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Summary: | Ulcerative colitis (UC) is a common inflammatory bowel disease, whose incidence is on the rise worldwide. The drugs commonly used for UC are often associated with a number of side effects. Therefore, the development of effective, food-borne substances for UC is in line with the current needs. Egg yolk phosphatidylcholine (EYPC) is one of the abundant lipids in egg yolk and possesses various biological activities. However, its protective effect against UC has not been clarified. In this study, the anti-UC activity of EYPC was investigated using a dextran sodium sulfate (DSS)-induced colitis model of BALB/c mice. The results showed that EYPC supplementation inhibited DSS-induced colon shortening, the spleen index and disease activity index increase and intestinal structural damage. EYPC could down-regulate the levels of TNF-α, IL-1β, IL-6 and MPO in the colon and restore the number of goblet cells and the level of tight junction (TJ) proteins. Besides, EYPC modulated the composition of the gut microbiota, lowered the relative abundance of the pathogenic bacterium
Parabacteroides
and upregulated the abundance of the beneficial bacteria
Alistipes
and
Lachnospiraceae_NK4A136_group
. These results evidenced that EYPC could attenuate DSS-induced colitis in mice and had the potential to prevent and treat UC.
EYPC alleviates DSS-induced colitis in mice by reducing inflammatory response, protecting intestinal barrier, and regulating gut microbiota. |
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Bibliography: | Electronic supplementary information (ESI) available. See DOI https://doi.org/10.1039/d3fo02885b ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2042-6496 2042-650X |
DOI: | 10.1039/d3fo02885b |