Ulcerative colitis (UC) is a chronic
intestinal disease with unclear pathogenesis. With an increasing global prevalence over the past two decades, UC poses a serious threat to public health. Baitouweng decoction (BTW), a
traditional Chinese medicine, has been shown to have good clinical efficacy for treating intestinal
inflammation. Yet, the efficacy of BTW in UC and the underlying mechanism remain unclear. The current study aimed to determine whether BTW suppressed intestinal
inflammation in mice and the potential mechanism. We used a
dextran sulfate sodium (DSS)-induced murine
colitis model to test the anti-inflammatory efficacy of BTW. Clinical symptoms were scored by the disease activity index (DAI), and the colon length and pathological changes in colon tissue were also used to further evaluate the efficacy of BTW. Precisely how BTW affected immune function and the intestinal barrier of UC mice was also examined. BTW significantly reduced DAI score and colonic pathological damage. BTW regulated the balance between T helper (Th)17 and regulatory T (Treg) cells, decreased
interleukin (IL)-1β,
IL-6, and
tumor necrosis factor-α, and increased
IL-10 levels. BTW reduced intestinal permeability of UC mice, increased expression of
tight junction proteins (
occludin and zonula occludens-1), and decreased expression of phospho-nuclear factor (p-NF)-κB and phospho-
extracellular signal-regulated kinase (p-ERK) in the colon. BTW inhibited the ERK/p-NF-κB signaling pathway and suppressed expression of cyclo-oxygenase-2 and inducible
NO synthase in
lipopolysaccharide-activated RAW 264.7 cells. BTW significantly promoted the synthesis of
short-chain fatty acids in the gut, particularly
acetate,
propionate,
isobutyric acid, and isovalerate. The results suggest that BTW can protect against DSS-induced UC. The mechanism may be partially attributed to regulating the balance of Th17/Treg cells and restoring the intestinal epithelial barrier.