In vivo, low-dose GdCl<sub>3</sub> improved colitis scores and inhibited acute phagocyte recruitment and colon damage within the mucosa as revealed by the decrease in MPO, nitric oxide (NO), and malondialdehyde (MDA) levels.
Meanwhile, the oxidative stress indicated by myeloperoxidase (MPO), reduced glutathione (GSH), malondialdehyde (MDA), and serum nitrate (NO) concentrations was higher in mice with DSS-induced colitis than in the control group mice, but dietary Q or Q+MQ supplementation counteracted this trend.
DAI evaluation, colon length, colon tissue morphology, histologic damage scores and relative protein concentrations (MPO, TNF-α and IL-1β) demonstrated that the Alg/Chi/IL-1Ra microcapsules alleviated DSS-induced colitis in mice.
Orally administered irisolidone or kakkalide alleviated colon shortening and myeloperoxidase activity in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis.
In a chronic colitis model, CEC more strongly decreased signs of colitis severity (myeloperoxidase activity and CD3<sup>+</sup> immune-cell infiltration) than Nissle.
TNBS significantly elevated myeloperoxidase (MPO) expression, macroscopic scores, and colon shortening.Oral <i>L. sakei</i> 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).<i>L. sakei</i> S1 inhibited the expression of inflammatory cytokines IL-1β, IL-6 and TNF-α, induced by TNBS, but enhanced IL-10 expression.<i>L. sakei</i> S1 showed resistance to artificial digestive juices and adherence to intestinal epithelial Caco-2 cells.Thus, <i>L. sakei</i> S1 may inhibit the NF-κB pathway and be used as functional food to treat colitis.