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Abstract
Objective This study aimed to determine whether Danggui Buxue decoction (DGBX) can improve inflammatory bowel disease (IBD) by regulating immunity and promoting intestinal mucosal repair. Method Dextran sulfate sodium (DSS) was used to induce the IBD model. Drugs (DGBX or saline) were administered to mice, which were randomly divided into three groups (control, model, and experimental groups). Hematoxylin and eosin staining of intestinal tissues was conducted to observe for morphological changes. Changes in cytokines and immune cells in the intestinal tissues were detected by enzyme-linked immunosorbent assay and flow cytometry. Immunofluorescence techniques were used to assess the status of the intestinal mucosal repair. Results This study found that treatment with DGBX can effectively improve the inflammatory state and pathological structure of the IBD model. DGBX not only can significantly change the composition of intestinal mucosal immune cells and promote the regression of inflammation but also significantly increase the proliferation of intestinal epithelial cells and promote the rapid repair of intestinal mucosal barrier injury compared with the model group (p < 0.05). Conclusion Taking these results, DGBX shows promising protective effects on IBD by regulating immunity and promoting intestinal mucosal repair.
Highlights
Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn’s disease, is characterized by chronic, recurrent gastrointestinal inflammation [1]
Mice were divided into three groups: the group that was fed with drinking water and given normal saline intragastrically, the group that was fed with Dextran sulfate sodium (DSS) water to induce enteritis and given DGBX intragastrically (Figure 1(a)), and the group that was given normal saline intragastrically during DSS induction
We killed the mice on day 9 and measured the length of the colon in each group. e results showed that the colon length was significantly lower in the DSS group than in the drinking water group, and the colon length was significantly longer in the DGBX group than in the DSS group (Figures 3(c) and 3(d))
Summary
Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn’s disease, is characterized by chronic, recurrent gastrointestinal inflammation [1]. During the onset of IBD, the imbalance of intestinal mucosal immunity and the destruction of the intestinal epithelial barrier function play an important role [5, 6]. Various immune cell populations, including macrophages, dendritic cells (DCs), neutrophils, and eosinophils in intestinal mucosa may aggravate inflammation during IBD [7]. Regulatory T cells (Tregs) limit IBD inflammation via immunosuppression; the metastasis of Tregs can eliminate the development of experimental colitis [8]. Is process causes damage to the Evidence-Based Complementary and Alternative Medicine intestinal epithelial cells and the destruction of the intestinal barrier function, leading to the occurrence and development of IBD [12, 13] Intestinal epithelial cells comprise the primary barrier that protects the body. e imbalance of the intestinal mucosal immunity results in a large number of inflammatory factors such as IL-1β, TNF-a, IL-6, IL-10, and IL-17A. is process causes damage to the Evidence-Based Complementary and Alternative Medicine intestinal epithelial cells and the destruction of the intestinal barrier function, leading to the occurrence and development of IBD [12, 13]
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