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Anthocyanins inhibit tumor necrosis alpha-induced loss of Caco-2 cell barrier integrity

Cremonini, Eleonora, Mastaloudis, Angela, Hester, Shelly N., Verstraeten, Sandra V., Anderson, Maureen, Wood, Steven M., Waterhouse, Andrew L., Fraga, Cesar G., Oteiza, Patricia I.
Food & function 2017 v.8 no.8 pp. 2915-2923
cyanidin, delphinidin, electrical resistance, human cell lines, inflammation, intestinal mucosa, malvidin, pathophysiology, permeability, petunidin, phosphorylation, plant extracts, rice, transcription factor NF-kappa B, tumor necrosis factor-alpha
An increased permeability of the intestinal barrier is proposed as a major event in the pathophysiology of conditions characterized by chronic gut inflammation. This study investigated the capacity of pure anthocyanins (AC), and berry and rice extracts containing different types and amounts of AC, to inhibit tumor necrosis alpha (TNFα)-induced permeabilization of Caco-2 cell monolayers. Caco-2 cells differentiated into intestinal epithelial cell monolayers were incubated in the absence/presence of TNFα, with or without the addition of AC or AC-rich plant extracts (ACRE). AC and ACRE inhibited TNFα-induced loss of monolayer permeability as assessed by changes in transepithelial electrical resistance (TEER) and paracellular transport of FITC-dextran. In the range of concentrations tested (0.25–1 μM), O-glucosides of cyanidin, and delphinidin, but not those of malvidin, peonidin and petunidin protected the monolayer from TNFα-induced decrease of TEER and increase of FITC-dextran permeability. Cyanidin and delphinidin acted by mitigating TNFα-triggered activation of transcription factor NF-κB, and downstream phosphorylation of myosin light chain (MLC). The protective actions of the ACRE on TNFα-induced TEER increase was positively correlated with the sum of cyanidins and delphinidins (r² = 0.83) content in the ACRE. However, no correlation was observed between TEER and ACRE total AC, malvidin, or peonidin content. Results support a particular capacity of cyanidins and delphinidins in the protection of the intestinal barrier against inflammation-induced permeabilization, in part through the inhibition of the NF-κB pathway.