ABSTRACT UC is a globally escalating intestinal disorder with limited safe and effective interventions. This study investigated the synergistic therapeutic effects and mechanisms of Lactobacillus johnsonii 46 ( L. johnsonii 46) (a feruloyl esterase‐producing strain) and rice bran (LJRB) on DSS‐induced UC in C57BL/6J mice. The animal groups were divided into control group (CON), DSS group (MOD), sulfasalazine group (SUL), rice bran group (RBN), L. johnsonii 46 group (LAJ), and LJRB treatment group (RBL). The organ index, disease index, and biochemical indicators of mice were measured, the histopathology of the colon was analyzed. The expression of inflammatory factor, tight junction protein and TLRs/TRAF6/NF‐κB signaling pathway genes were detected by Real‐Time Quantitative Polymerase Chain Reaction (RT‐qPCR). LJRB supplementation exerted superior protective effects compared to single rice bran (RBN) or L. johnsonii 46 (LAJ) intervention: it significantly alleviated DSS‐induced weight loss (RBL group: 1.46 ± 0.21 g vs. MOD group: ∼3 g, p < 0.05), restored colon length, and reduced the disease activity index (DAI) by ∼50%. Biochemical and molecular analyses showed LJRB remarkably suppressed serum pro‐inflammatory cytokines (IL‐1β, TNF‐α, IL‐6; 40%–60% reduction vs. MOD group) while elevating anti‐inflammatory IL‐10 (∼35% increase), enhanced colonic antioxidant capacity (reduced MDA by ∼30% and increased SOD, GSH, GSH‐Px by 25%–40%), and enriched cecal short‐chain fatty acids (SCFAs) with acetic acid (0.99 µmol/g), propionic acid (0.31 µmol/g), and butyric acid (0.21 µmol/g) significantly higher than the MOD group. Mechanistically, LJRB synergistically inhibited the TLRs/TRAF6/NF‐κB signaling pathway, as indicated by downregulated mRNA expression of TLR4, MyD88, IKKβ, and NF‐κB p65 (30%–50% reduction vs. MOD group) and decreased phosphorylation of IKKβ, IκBα, and NF‐κB p65 proteins. Histopathological observations confirmed LJRB preserved colon tissue integrity, reduced goblet cell loss, and alleviated mucosal erosion and edema. Collectively, these findings demonstrate LJRB alleviates UC through multi‐targeted mechanisms (anti‐inflammation, antioxidation, SCFA production promotion, and nuclear factor kappa‐B (NF‐κB) pathway inhibition), highlighting its potential as a novel natural dietary supplement for UC prevention and management.
Lu et al. (Sun,) studied this question.