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Dietary Gangliosides Improve Intestinal Integrity and Function by Decreasing sPLA2 Independent NF‐kB Activation Mechanism in a Caco‐2 Cell Model of IBD by DSS
Author(s) -
Li Qun,
Thomsom Alan B.R.,
Mazurak Vera C.,
Field Catherine J.,
Clandinin M. Tom
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1033.11
Subject(s) - ganglioside , barrier function , ceramide , caco 2 , chemistry , sialic acid , microbiology and biotechnology , tight junction , cell , sphingolipid , biochemistry , biology , apoptosis
Gangliosides are negatively charged glycosphingolipids that consist of a hydrophobic ceramide and a hydrophilic oligosaccharide chain bearing one or more sialic acid. Both animal and human cell studies suggest that gangliosides have anti‐inflammatory effects by modulating cytokine expression. The objective of this study was to use Caco‐2 IBD model induced by dextran sulfate sodium to investigate benefits of ganglioside supplementation on IBD signaling mechanisms. Epithelial barrier function was examined by measuring TEER and intestinal morphological structure damage was studied via TEM. HBD‐2, sPLA2 and NF‐kB was determined by ELISA methods. Results indicated that supplementary ganglioside significantly decreased inflammatory HBD‐2 level, improved the defective epithelial barrier function and protected the disruption of intestinal junction complexes. The sPLA2 level in the basolateral medium was significantly decreased in ganglioside supplemented cells by 40%. NF‐kB P65 activation was significantly increased by DSS alone or with ganglioside supplement. In conclusion, the present study indicated that ganglioside has promising beneficial effects on IBD by decreasing inflammatory signaling, improving epithelial barrier function and protecting intestinal integrity. The anti‐inflammatory effect may also partly contribute to decrease of sPLA2 level, while independent of NF‐kB activation. Grant Funding Source : CIHR