Alleviating effects of tumorous stem mustard fermented by starter cultures on ulcerative colitis through modulating gut microbiota and inhibiting the TLR4/MyD88/NF-κB pathway

Tumorous stem mustard (TSM) is one kind of important cruciferous vegetables for directly consumption and processing in China. Inoculation of lactic acid bacteria (LAB) starters can enhance the maturing of fermented vegetables and improve the sensory quality. However, it is unknown whether homo- and hetero-fermentative LAB starters exert distinct effects on the functional activities of fermented vegetables. Fermented with homo-fermentative Lactiplantibacillus plantarum S7-12 and heterofermentative Lentilactobacillus parafarraginis L-7 enhanced the ripening of fermented tumorous stem mustard (FTSM), improved the glucosinolate contents and showed higher antioxidant activities than spontaneous fermentation TSM. Apart from the differences in the production of organic acids, S7-12 starter retained higher content of total phenolics than L-7. Furthermore, FTSM treatment alleviated the DSS-induced colitis symptoms including body weight loss, DAI values and shortened colonic length. Both S7-12 and L-7 FTSM better ameliorated colonic pathological damage and exhibited good antioxidative activity in vivo than SF FTSM, but there was no significant difference between them. Immunohistochemical results further confirmed that FTSM maintained the colon mucosal barrier function by restoring TJ proteins. Moreover, FTSM supplementation could reduce the levels of serum and colonic proinflammatory cytokines IL-6, TNF-α and IL-1β and enhance the expression of anti-inflammatory cytokine IL-10 by inhibiting the TLR4/MyD88/NF-κB signaling pathway. FTSM treatment reversed the decline in the microbial diversity induced by DSS and reduced the pro-inflammatory gram-negative bacteria Enterobacteriaceae. In conclusion, S7-12 and L-7-inoculated FTSM relieved the DSS-induced colitis through regulating the composition of intestinal microbiota and inhibiting the TLR4/MyD88/NF-κB signaling pathway.