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Published in: Digestive Diseases and Sciences 2/2012

01-02-2012 | Original Article

Dietary Kaempferol Suppresses Inflammation of Dextran Sulfate Sodium-Induced Colitis in Mice

Authors: Mi-Young Park, Geun Eog Ji, Mi-Kyung Sung

Published in: Digestive Diseases and Sciences | Issue 2/2012

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Abstract

Background

In ulcerative colitis (UC), reduction of inflammation may represent a key mechanism in UC therapy, and anti-inflammatory agents would be good candidates for preventing UC. Kaempferol, a natural flavonoid, is believed to have anti-inflammatory activities and has been shown to be potentially immune-modulatory.

Aims

The aim of this study was to determine whether kaempferol alleviates the inflammatory responses of dextran sulfate sodium (DSS)-induced colitis in mice.

Methods

Female C57BL/6J mice were divided into six groups: a negative control group, a DSS control group, and DSS + 0.1% or 0.3% kaempferol pre- or post-fed groups. At the end of the experimental period, clinical and biochemical markers were evaluated.

Results

Plasma levels of NO and PGE2 were significantly decreased in both the 0.3% kaempferol pre- and post-fed groups. The plasma LTB4 level was profoundly decreased in all animals fed kaempferol. Colonic mucosa MPO activity was also suppressed in both the 0.3% kaempferol pre- or post-fed groups. TFF3 mRNA, a marker for goblet cell function, was up-regulated in kaempferol pre-fed animals.

Conclusions

These results indicate that kaempferol is an effective anti-inflammatory agent that protects colonic mucosa from DSS-induced UC. Dietary kaempferol fed prior to colitis induction was more effective to suppress some of the colitis-associated markers.
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Metadata
Title
Dietary Kaempferol Suppresses Inflammation of Dextran Sulfate Sodium-Induced Colitis in Mice
Authors
Mi-Young Park
Geun Eog Ji
Mi-Kyung Sung
Publication date
01-02-2012
Publisher
Springer US
Published in
Digestive Diseases and Sciences / Issue 2/2012
Print ISSN: 0163-2116
Electronic ISSN: 1573-2568
DOI
https://doi.org/10.1007/s10620-011-1883-8

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