Abstract
Ulcerative colitis (UC) is a chronic inflammatory disease. Here, the potential effects of Capparis spinosa water extract (CSWE) on colonic histopathology, inflammation, and gut microbiota composition in dextran sulfate sodium (DSS) induced UC mice were evaluated. Our results showed that CSWE treatment improved the colonic histopathology of UC mice, increased the levels of tight junction protein gene ZO-1 and Occludin in intestinal epithelial cells, and inhibited the expression of proinflammatory cytokines (IL-1β, IL-6, and TNF-α). Furthermore, CSWE administration alleviated oxidative stress in the colon of UC mice. The effects of CSWE on the compositions and metabolomic profiles of the gut microbiota in UC mice were investigated. It was found that CSWE could enhance the diversity of gut microbes and the abundance of probiotics and metabonomics had the strongest association with Firmicutes. Our results indicated that CSWE might be an ideal candidate as a potential therapeutic natural product for the treatment of UC.
Highlights
Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease, is an idiopathic, chronic, and recurrent disease [1]
The colon length was significantly shorter in the mice in the dextran sulfate sodium (DSS) group than in mice in the other groups, while the colonic shortening induced by DSS was restored in a dose-dependent manner by C. spinosa water extract (CSWE) (Figures 1(c) and 1(d))
A growing body of research has reported that the polysaccharides present in many traditional Chinese medicines, such as Tremella fuciformis polysaccharides [23] and Atractylodes macrocephala polysaccharides [19], play a crucial role in the treatment of UC
Summary
Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease, is an idiopathic, chronic, and recurrent disease [1]. UC is a chronic inflammatory disease characterized by mucosal inflammation of the colon and rectum, with typical symptoms of rectal bleeding, diarrhea, and urgency [2]. It has been reported that UC can be triggered and proceed through the interaction of genetic factors, environmental factors such as stress and food habits, excessive production of inflammation-related cytokines, and abnormal immune responses in the mucosal and submucosal layers of the intestine [5]. Despite the availability of various therapeutic agents for the treatment of UC, routine treatment has limitations and serious side effects, such as drug dependence, disruption of the immune system, and irreversible complications, including hypertension and gastric ulcer [7]
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