Sodium new houttuyfonate improves inflammatory bowel disease in mice through inhibiting the STAT3/NF-κB signaling pathway

Objective To investigate the effects of sodium new houttuyfonate (SNH) on inflammatory bowel disease (IBD) in mice and regulatory effects on the STAT3/NF-κB signaling pathway. Methods A total of 24 mice were randomly divided into three groups: a blank control (CON) group, an IBD modeling (IBD) group and an intervention (SNH) group. Mice in the IBD and SNH groups were given 3% dextran sulfate sodium salt (DSS) in drinking water for modeling. Furthermore, the SNH group was administered with SNH by gavage, while both the CON and IBD groups were administered with normal saline by gavage, for consecutive two weeks. The body weight, fecal consistency and hematochezia of mice in each group were observed daily for measurement of disease activity index (DAI). The pathological changes of the colon tissue in mice of each group were detected by H-E staining. The levels of STAT3 and NF-κB in colon tissue were measured by Western blot. The levels of serum interleukin (IL)-6, tumor necrosis factor (TNF)-α and IL-18 were detected by ELISA. Results SNH treatment significantly increased the body weights of mice in the IBD group (P＜0.05), relieved diarrhea, hematochezia and colon tissue damage, and reduced DAI in IBD mice (P＜0.05). According to H-E staining, SNH relieved the pathological damage of colon tissues in IBD mice to some extent. Compared with the CON group, the IBD group produced remarkably increased levels of STAT3 and NF-κB in colon tissue (P<0.05). Moreover, compared with the IBD group, the SNH group produced remarkably decreased levels of STAT3 and NF-κB in colon tissue (P<0.05). Furthermore, the levels of IL-6, TNF-α and IL-18 obviously increased in the IBD group (P<0.05), which were reduced after SNH treatment in the SNH group (P<0.05). Conclusions SNH can suppress intestinal inflammation caused by DSS in mice, which may be associated with inhibiting the STAT3/NF-κB pathway, so as to reduce the levels of IL-6,TNF-α and IL-18.