As a processing by-product, green pea hull (GPH) was found to be rich in phenolic components in our previous studies. In this study, UHPLC-LTQ-OrbiTrap-MS (Ultra performance liquid chromatography-linear ion trap orbitrap tandem mass spectrometry) technique was used to quantify polyphenols, and DSS (sodium dextran sulfate)-induced colitis mouse model was established to explore the effect of GPH extracts on colitis. The results showed that quercetin and its derivatives, kaempferol trihexanside and catechin and its derivatives were the main phenolic substances in the extract, reaching 2836.57, 1482.00 and 1339.91 µg quercetin/g GPH extract, respectively; GPH extracts can improved inflammatory status, repaired colonic function, regulated inflammatory factors, and restored oxidative balance in mice. Further, GPH extracts can activate Keap1-Nrf2-ARE signaling pathway, regulate downstream antioxidant protease and gut microbiota by increasing F/B value and promoting the growth of Lactobacillaceae and Lachnospiraceae, and improve the level of SCFAs (short-chain fatty acids) to relieve DSS-induced colitis in mice. Therefore, GPH may be a promising dietary resource for the treatment of ulcerative colitis.

The fruit of Akebia trifoliata is popular in Asia, but researches concerning the phytochemicals of A. trifoliate pericarp extract (APE) and their metabolites, bioavailability, metabolism and anti-inflammatory activity in vivo are less known. In the present study, the chemical constituents of APE and their metabolites of rats after oral administration were identified using UPLC-LTQ-Orbitrap-MS/MS. A total of 18 compounds were tentatively characterized in APE, while 8 original compounds and 8 metabolites were observed in plasma, and 10 original compounds and 39 metabolites were detected in urine. Deglycosylation, glucuronidation, methylation and sulfation were the reactions that mainly occurred in the metabolism in vivo. Meanwhile, APE supplementation decreased dextran sulphate sodium (DSS)-induced colitis in mice, ameliorating epithelial barrier disruption, suppressing the proliferation and infiltration of immune cells, modulating the secretion of nitric oxide (NO) and prostaglandin E₂ (PGE₂), decreasing the expression of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as regulating oxidative stress in vivo. The results suggested that APE triterpenoids and their metabolites as major contributors to anti-inflammatory activities, providing a scientific basis for the use of APE as a functional food to ameliorate colon health in humans.

Akebia trifoliata fruits, a kind of popular edible berry in Asia, are widely consumed as daily fruits or functional foods. Our previous study found several bioactives from Akebia trifoliata pericarp extract (APE), and preliminarily investigated their anti-inflammatory activity. However, the underlying mechanism of APE for the observed anti-inflammatory effects is still unknown. Thus, the bioactive profiles and anti-inflammatory mechanism of APE were investigated by a combination of chemical assays: UPLC-LTQ-Orbitrap/MS technique, lipopolysaccharide (LPS)-induced RAW264.7 cells and DSS-induced mouse model. The results indicated that the phenolic acids and terpenoids are major bioactives of APE, which could inhibit the production of nitric oxide (NO) and prostaglandin E2 (PGE₂) by blocking the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in RAW264.7 cells as well as reduce the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), and suppress the phosphorylation of p-65, IκBα and mitogen-activated protein kinase (MAPKs including p38, ERKs, JNKs) proteins both in vitro and in vivo. Furthermore, APE treatment could regulate gut microbiota by increasing the richness of Rikenellaceae and Lactobacillaceae and reducing that of Lachnospiraceae and Ruminococcaceae. In summary, these findings clearly demonstrated that APE mitigates inflammation by restraining the production of cytokines through nuclear factor-κB (NF-κB) and MAPK signaling pathways, and altering gut microbiota, and therefore, this could be a potential functional food for the treatment and prevention of inflammatory bowel diseases.

Tetrastigma hemsleyanum, a precious edible and medicinal plant in China, has attracted extensive research attention in recent years due to its high traditional value for the treatment of various diseases. In vitro digestion and colonic fermentation models were established to evaluate the stability of Tetrastigma hemsleyanum leaves (THL) phenolics by the HPLC-QqQ-MS/MS method. The total phenolic and flavonoid contents were degraded during digestion and fermentation. 3-caffeoylquinic acid, 5-caffeoylquinic acid, orientin and (iso)vitexin were metabolized by digestive enzymes and the gut microbiota, and absorbed in the form of glycosides and smaller phenolic acids for hepatic metabolism. The protective effects of THL on dextran sodium sulfate (DSS)-induced colitis in mice and potential mechanisms were explored. The results showed that THL supplementation increased the body weight and colon length, and the expression levels of tight junction proteins including occludin, claudin-1 and ZO-1 were up-regulated by THL. The secretions of pro-inflammatory cytokines containing IL-1β, IL-6 and TNF-α were significantly suppressed, whereas the content of anti-inflammatory cytokine IL-10 was promoted in the THL treated group. In addition, THL treatment activated the nuclear transfer of Nrf2, improved the expression of SOD, CAT, HO-1, NQO1 and GCLC, and decreased the content of MPO and MDA. It is worth noting that THL treatment significantly increased the content of short-chain fatty acids (SCFAs), increased the abundance of Ruminococcaceae, and decreased the abundance of Verrucomicrobia which is positively correlated with pro-inflammatory cytokines. These results indicated that THL effectively inhibited DSS-induced colitis by maintaining the intestinal epithelial barrier, mitigated oxidative stress through regulating the Keap1/Nrf2 signaling pathway and regulated the imbalance of the intestinal flora structure.