Effects of food matrix elements (dietary fibres) on grapefruit peel flavanone profile and on faecal microbiota during in vitro fermentation.

Citrus fruits are a good source of flavanones. The present study aimed to assess the effect of food matrix elements [dietary fibres (DFs)] on the flavanone profile of grapefruit peel (GFP) and on the gut microbiota during in vitro digestion and simulated colonic fermentation. The contents of low-molecular-weight metabolites (dihydrocaffeic acid and 3-phenylpropionic acid) were increased by pectin, konjac and chitosan in medium- and high-viscosity matrices. Compared with the GFP group, the counts of Lactobacillus spp. and Clostridium leptum were significantly increased in medium-viscosity food matrices (konjac and chitosan) (p < 0.05). Moreover, the acetic and propionic acid contents were significantly elevated in the GFP + DF groups after 12 h of fermentation (p < 0.05). GFP flavanones were retained by DF, and the total phenolic content (TPC) and antioxidant potency composite (APC) index decreased during in vitro digestion. These findings indicate that medium-viscosity DFs (konjac and chitosan) could act as key food matrix elements for the retention of polyphenols.

Regulatory effects of flavonoids luteolin on BDE-209-induced intestinal epithelial barrier damage in Caco-2 cell monolayer model.

Polybrominated diphenyl ethers (PBDEs) are persistent organic pollutants (POPs). They are constantly detected in foods. PBDEs can disrupt the intestinal flora, but enterotoxicity is unknown. Luteolin, one kind of flavonoid, has drawn increasing interest as an agent that strengthens the intestinal barrier. This study aimed to evaluate the mitigating effect of luteolin on damage to the intestinal barrier induced by decabromodiphenyl ether (BDE-209) in a Caco-2 cell monolayer model. Results showed that luteolin mitigated BDE-209-induced damage to intestinal epithelial barrier by reducing the levels of reactive oxygen species (ROS), increasing the activity of superoxide dismutase (SOD) and glutathione (GSH), suppressed the secretion of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1ß), and increased the expression of tight junction (TJ) proteins (ZO-1, occludin, and claudin-1). Furthermore, the protective effects were related to the inhibition of extracellular regulated protein kinases (ERK) and nuclear factor kappa-B (NF-κB)/myosin light chain kinase (MLCK) signaling pathways, and the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways. This study is the first to provide strong evidence that BDE-209 can damage the intestinal barrier, and we here investigated the important protective effect of luteolin, which may lay the foundation for the development of luteolin as a dietary supplement to strengthen the intestinal barrier.

Chlorogenic acid attenuates cadmium-induced intestinal injury in Sprague-Dawley rats.

Chronic exposure to cadmium (Cd) causes remarkable damage to the liver and gastrointestinal tract. Previous studies have revealed that chlorogenic acid (CGA) could improve the intestinal barrier integrity for weaned rats. Hence, this study sought to investigate the protective effects of CGA from pure reagent and sunflower seed extract (SSE) on growth performance, antioxidant indicators, inflammatory biomarkers and intestinal barrier function in Cd treated rats. A total of 32 Sprague-Dawley female rats with similar weights were randomly allotted to four treatments: control, CdCl2 (6 mg/kg BW), co-treatment of Cd (6 mg/kg BW) and pure CGA (50 mg/kg BW), and co-treatment of Cd (6 mg/kg BW) and SSE (50 mg/kg BW) for 14 days. The data indicated that, CGA or SSE with Cd sequestration and good antioxidative ability decreased Cd absorption and accumulation in the jejunum and increased fecal Cd levels in Cd-exposed rats. Compared with the Cd group, co-treatment with CGA or SSE also alleviated inflammation, ameliorated the villus damage, reversed the disruption of tight junctions, and recovered weight gain of rats. These results suggest that CGA or SSE can protect the intestinal barrier, which is related to the alleviation of Cd-induced oxidative stress and growth decrease.