Alleviation effects of <i>Lactobacillus plantarum</i> in colitis aggravated by a high-salt diet depend on intestinal barrier protection, NF-κB pathway regulation, and oxidative stress improvement

A high-salt diet (HSD) can result in numerous health issues, including exacerbation of intestinal inflammation. Therefore, there is an immediate necessity of developing dietary supplements that can mitigate colitis exacerbated by a HSD. This study examined the impact of <i>Lactobacillus plantarum</i> HGD228 on colitis exacerbated by a HSD and the mechanisms underlying its alleviation. HGD228 treatment significantly enhanced colonic goblet cells and MUC2, upregulated ZO-1 and occludin, inhibited epithelial cell apoptosis, and mitigated colitis exacerbated by a HSD. Moreover, HGD228 significantly regulated oxidative stress-related enzymes, including SOD, GSH-PX, and CAT. HGD228 treatment significantly suppressed the NF-κB pathway induced by a HSD and regulated the levels of cytokines, including TNF-α, IL-10, and IL-1β. Furthermore, HGD228 reestablished the gut microbiota altered by HSDDSS, increasing <i>Bifidobacterium</i> while decreasing <i>Escherichia</i>-<i>Shigella</i> and <i>Clostridium sensu stricto 1</i>. HGD228 treatment also enhanced the production of butyric acid and acetic acid, suppressed pro-inflammatory cytokines, and strengthened the intestinal mucosal barrier. Therefore, HGD228 enhanced the production of beneficial metabolites by regulating inflammatory cytokines and oxidative stress, preserving the mucosal barrier, and enhancing gut microbiota, and mitigated colitis aggravated by a HSD. These results will aid in clinical trials of probiotics and the development of dietary supplements for colitis, with promising application value.