The intestinal mucosa is the intestinal lumen tissue that protects the intestine from invasion, maintains intestinal barrier function, and participates in the immune response. Diseases such as inflammatory enteritis and intestinal infections can cause damage to the intestinal mucosal barrier and dysfunction. The aim of this study was to investigate the improvement mechanism of malvidin-3-O-galactoside (M3G) on small intestinal mucosal barrier function. C57BL/6J male mice were given dextran sodium sulfate (DSS) for 7 days to induce enteritis, and then were fed normally with or with M3G supplementation for another 7 days. The results showed that M3G supplementation significantly improved the disease activity index (DAI) score and small intestinal tissue injury in mice with DSS induced enteritis. M3G ameliorated the small intestinal mucosal mechanical barrier function by modulating the expression of mucin2 (MUC2), zona occludens 1 (ZO-1), Occludin, Claudin-1, intestinal fatty acid binding protein (iFABP), and trefoil factor 3 (TFF3) in the small intestine mucosa, and the serum levels of D-lactic acid (D-LA), lipopolysaccharide (LPS), and diamine oxidase (DAO) were significantly decreased. Additionally, M3G also relieved the small intestinal immunologic barrier of mice by decreasing the immune protein levels of immunoglobulin A (IgA), immunoglobulin M (IgM), and immunoglobulin G (IgG) in serum, and secretory immunoglobulin A (SIgA) level in small intestine tissue. Furthermore, M3G inhibited the expression of Notch pathway-related proteins such as Notch1, notch intracellular domain (NICD), delta-like ligand 4 (DLL4), delta-like ligand 1 (DLL1), and hairy/enhancer of split 1 (Hes1). In conclusion, the results demonstrated that M3G can improve intestinal mucosal barrier function by inhibiting Notch pathway.
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High-fat diet (HFD) induces imbalance in the small intestine environment, where fat digestion and absorption mainly take place. This study aimed to elucidate the mechanisms by which Lonicera caerulea polyphenols (LCP) might inhibit fat absorption, from the perspective of small intestine microbiota and epithelial barrier integrity.
Male Sprague-Dawley rats were given HFD with or without co-administration of LCP for 8 weeks. The results showed that LCP supplementation significantly decreased the levels of serum triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C), and increased the contents of fecal sterols, in HFD rats. LCP also inhibited the dysfunction of the small intestine epithelial barrier, via alleviating the oxidative stress activated by Nrf2-ARE pathway, and by modulating the expressions of pro-inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), cyclooxygenase-2 (COX-2), nuclear factor kappa-B p65 (NF-κB p65) and inducible nitric oxide synthase (iNOS) in the small intestine. Additionally, LCP administration restored the balance in small intestine microbiota and increased the abundance of the specific bacteria, such as Lactobacillus, involved in fat absorption.
Our results demonstrated that LCP may be beneficial to inhibit fat absorption. The mechanism seems to be associated with the protection of the epithelial barrier integrity and the modulation of specific bacteria in the small intestine.
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