Pea Albumin Attenuates Dextran Sulfate Sodium-Induced Colitis by Regulating NF-κB Signaling and the Intestinal Microbiota in Mice

Background: Inflammatory bowel disease remains a global burden with rapidly increasing incidence and prevalence in both industrialized countries and developing countries. In this study, we prepared pea albumin from pea seeds and determined its beneficial effects being anti-inflammatory and on gut microbiota modulation in dextran sulfate sodium (DSS)-challenged mice. Method: Six-week-old C57BL/6N male mice received an equivalent volume (200 μL) of sterile phosphate balanced solution, 0.375, 0.75, or 1.50 g/kg body weight (BW) of pea albumin that was subjected to 2.0% DSS for 7 days to induce colitis. On day 17 of the experiment, all mice were sacrificed after blood sample collection, and colon tissue and colon contents were collected. BW change curve, colon length, myeloperoxidase (MPO) activity, mucus staining, immunofluorescence staining of T cells and macrophages, cytokines, pro-inflammatory genes expression, nuclear factor-κB (NF-κB) and signal transducer, and activator of transcription 3 (STAT3) signaling pathways as well as 16S DNA sequence were measured. Results: Our results show that pea albumin alleviates DSS-induced BW loss, colon length shortening, enhanced MPO activity, cytokines secretion, mucus deficiency, and inflammatory cell infiltration, as well as enhanced pro-inflammatory genes expression. In addition, the overactivation of NF-κB and STAT3 following DSS exposure is attenuated by pea albumin administration. Of particular interest, pea albumin oral administration restored gut microbiota dysbiosis as evidenced by enhanced α-diversity, restored β-diversity, and promoted relative abundance of Lactobacillus and Lachnospiraceae_NK4A136_group. Conclusion: Taken together, the data provided herein demonstrated that pea albumin plays a protective role in DSS-induced colitis by reducing inflammatory cell infiltration, pro-inflammatory genes expression and pro-inflammatory cytokines release, inactivation of NF-κB signal, and gut microbiota modulation.