S1 Improves Colitis Induced by 2,4,6-Trinitrobenzene Sulfonic Acid by the Inhibition of NF-κB Signaling in Mice.

S1 strongly inhibits the expression of interleukin (IL)-6 and IL-1β in lipopolysaccharide-induced peritoneal macrophages by a mechanism for which lactic acid bacteria from kimchi that inhibit tumor necrosis factor-alpha (TNF-κ) were isolated. Therefore, we further evaluated the protective effect of this strain on the colitis mouse model induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS). TNBS significantly elevated myeloperoxidase (MPO) expression, macroscopic scores, and colon shortening. Oral S1 administration resulted in reduction of TNBS-induced loss in body weight, colon shortening, MPO activity, expression of cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS) and nuclear factor-kappa B (NF-κB). S1 inhibited the expression of inflammatory cytokines IL-1β, IL-6 and TNF-κ, induced by TNBS, but enhanced IL-10 expression. S1 showed resistance to artificial digestive juices and adherence to intestinal epithelial Caco-2 cells. Thus, S1 may inhibit the NF-κB pathway and be used in functional food to treat colitis.