Abstract:
:An increased permeability of the intestinal barrier is proposed as a major event in the pathophysiology of inflammatory bowel diseases (IBD). Tumor necrosis alpha (TNFα) plays a central role in IBD pathogenesis, in part promoting tight function (TJ) barrier dysfunction. Food extracts enriched in (-)-epicatechin (EC) prevent the development or improve the progression of IBD in animal models. This study investigated the capacity of EC to inhibit TNFα-induced permeabilization of Caco-2 cell monolayers, characterizing the underlying mechanisms. Caco-2 cells differentiated into intestinal epithelial cells were incubated in the absence/presence of TNFα, with or without the addition of 0.5-5 μM EC. TNFα triggered cell monolayer permeabilization, decreasing transepithelial electrical resistance (TEER) and increasing the paracellular transport of fluorescein sulfonic acid. The permeabilizing effects of TNFα were not due to Caco-2 cell apoptosis as evaluated by DNA fragmentation, caspase 3 and 9 activation, and cell morphology. EC prevented TNFα-triggered Caco-2 monolayer permeabilization and acted inhibiting the associated: (i) NADPH oxidase (NOX)-mediated increased oxidant production, (ii) NF-κB (IκBα phosphorylation, p50 and RelA nuclear transport, and nuclear NF-κB-DNA binding) and ERK1/2 activation, (iii) increased myosin light kinase expression, and decreased TJ protein ZO-1 levels. In summary, EC prevented TNFα-mediated Caco-2 cell barrier permeabilization in part through the inhibition of NOX/NF-κB activation and downstream TJ disruption. Diets rich in EC could contribute to ameliorate IBD-associated increased intestinal permeability.
journal_name
Arch Biochem Biophysjournal_title
Archives of biochemistry and biophysicsauthors
Contreras TC,Ricciardi E,Cremonini E,Oteiza PIdoi
10.1016/j.abb.2015.01.024subject
Has Abstractpub_date
2015-05-01 00:00:00pages
84-91eissn
0003-9861issn
1096-0384pii
S0003-9861(15)00049-1journal_volume
573pub_type
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