Clostridium butyricum (CB), a probiotic, is a gram-positive obligate anaerobic bacillus with
acid and heat resistant properties. Previous studies have reported that CB has beneficial effects in
intestinal diseases and regulates intestinal function. The aim of the present study was to investigate the protective effects and mechanisms of CB on the intestinal barrier function. Mice were randomly divided into three experimental groups (n=15 mice/group), including control,
dextran sodium sulfate (DSS) and DSS + CB. In the DSS and DSS + CB groups
colitis was induced with 3% DSS dissolved in
drinking water for 7 days. DSS + CB group mice were co-treated daily with 200 µl (2x108 CFU) CB
solution via gavage. The intestinal mucosal barrier function in mice was assessed by measuring
FITC-labeled 4-kDa
dextran (molecular weight, 4,000 Da) flux and by analyzing the expression of tight junction (TJ)-related
proteins using western blot analysis. In addition, the secretion levels of
tumor necrosis factor-α (TNF-α),
interleukin (IL)-1β,
IL-6,
IL-10 and
IL-13, and the concentration of
malondialdehyde,
glutathione and
superoxide dismutase were detected using ELISAs to determine
inflammation and oxidative stress, respectively. The activation status of the Akt/mTOR signaling pathway was also investigated using western blot analysis. The results demonstrated that, in mice with DSS-induced
colitis treatment, co-treatment with CB attenuated
colitis symptoms and intestinal permeability, increased the expression levels of TJ-related
proteins, decreased TNF-α, IL-1β and
IL-13 secretion levels but increased those of
IL-10, and reduced oxidative stress. Additionally, CB elevated the phosphorylation of Akt, mTOR and p70
ribosomal protein S6 kinase. Collectively, the present results indicated that CB protected intestinal barrier function and decreased intestinal mucosal permeability via upregulating the expression levels of TJ-related
proteins in a mouse model of DSS-induced
colitis. Moreover, the results suggested that the effects of CB could be mediated by the Akt/mTOR signaling pathway.