Blueberry and Raspberry powders mitigate Caco-2 cell monolayer permeabilization induced by TNF-α through the modulation of the inflammatory and oxidative stress process

Background and objectives: The impairment of the intestinal permeability (IP) leads to a low-grade and systemic inflammation which represents a risk for chronic diseases development. It has been postulated that polyphenol-rich foods such as berries, may play a beneficial effect against an increased IP. The aim of the present study was to evaluate the effect of blueberry (BB) and raspberry (RB) on Caco-2 cell monolayer permeabilization, inflammation and oxidative stress.~ Methods: Caco-2 cell monolayer permeabilization was evaluated by using Transwell model, measuring transepithelial electrical resistance (TEER) and paracellular transport of FITC (Fluorescein-5-isothiocyanate)-dextran in the absence/presence of TNF-α pro-inflammatory stimulus (10 ng/ml) and with or without the supplementation of BB and RB powders tested at different concentrations (1 and 5 mg/ml) for 24 hours. The total polyphenols (TPs) content ranged from 12 to 60 µg/ml for RB and from 55 to 275 µg/ml for BB, while total anthocyanins (ACNs) content ranged from 3 to 15 µg/ml for RB and from 11 to 55 µg/ml for BB. The expression of tight junction (TJ) proteins, inflammatory (IL-6 and TNF-α) and oxidative stress (8-hydroxy 2 deoxyguanosine) markers were measured in the supernatants or cell lysate in accordance to the instructions reported in the ELISA kits. Results: The results have documented that the incubation with BB and RB powders mitigated the loss of Caco-2 cell barrier integrity induced by TNF-α, reported as increased values in TEER and reduced values in FITC. However, this activity was dose and product dependent. In addition, a positive modulation of protein involved in IP such as claudin-1 and occludin was documented. Finally, BB and RB powders were able to counteract inflammation and oxidative stress. Conclusions: Our findings suggest the potential role of BB and RB to counteract in vitro an impairment of IP induced by TNF-α as pro-inflammatory stimulus. This beneficial effect seems to be potentially carried out through a modulation of the expression of TJ proteins, and a reduction of the oxidative stress and inflammation.