Abstract
Materials and Methods After intragastric administration of DOFP for 3 weeks, the rat UC model was made by the administration of 4% oral DSS solution for one week, and the drug was given at the same time. During the experiment, the disease activity index (DAI) score of the rats was regularly computed. At the end of the experiment, the blood routine indexes of rats were obtained. The histopathological changes in the colon were monitored by hematoxylin-eosin (H&E) and PAS staining and observation of ultrastructural changes in the colon by transmission electron microscope. Occludin expression in the colon was monitored by Western blot, the expression of claudin-1 and ZO-1 in the colon was detected by immunofluorescence, and the expression of TNF-α, IL-6, and IL-1β in the colon was detected by immunohistochemistry. Results The results firstly indicated that DOFP could significantly alleviate the signs and symptoms of the DSS-induced rats UC model, which manifested as improvement of body weight loss, increase of colon length, and improvement of the symptoms of diarrhea and hematochezia. Then, results from histopathology, blood routine examination, and transmission electron microscope analysis further implied that DOFP could dramatically reduce inflammatory cell infiltration and restore intestinal epithelial barrier integrity. In addition, the experiments of Western Blot analysis, immunofluorescence, and PAS staining also further confirmed that DOFP could markedly increase related protein expressions of the intestinal barrier and mucus barrier, as the expression of occludin, claudin-1, and ZO-1 in the colon significantly decreased. The experiments of immunohistochemistry confirmed that DOFP could markedly decrease protein expression levels of inflammatory cytokines TNF-α, IL-6, and IL-1β. Conclusion DOFP notably alleviated inflammatory lesions, repaired the colon mucosa damage by promoting the expression of tight junction proteins occludin, claudin-1, and ZO-1 and inhibiting the release of inflammatory factors TNF-α, IL-6, and IL-1β, and finally achieved the purpose of treating UC.
Highlights
Ulcerative colitis (UC) is an inflammatory bowel disease characterized by inflammatory cell infiltration into the colonic mucosa. e etiology and pathogenesis of ulcerative colitis are not clear [1, 2]. is disorder severely affects the normal life of patients and increases the risk of secondary infections and colon cancer [3]
Intestinal epithelial Tight junctions (TJs) protein can block the abnormal immune response caused by pathogenic intestinal microorganisms and alleviate the inflammatory response caused by excessive leakage of bacteria and antigens through the mucous membrane [8]. erefore, when there is a decrease in TJs, intestinal permeability increases, and this can cause celiac disease, diabetes, UC, and other diseases [10]
Compared with the model group, both high and low doses of D. officinale ultrafine powder (DOFP) improved the symptoms of colon shortening in model rats, and it significantly improved the disease activity index (DAI) score in model rats (P < 0.05). e above data indicated that DOFP treatment improved dextran sulfate sodium (DSS)-induced colitis in rats
Summary
Ulcerative colitis (UC) is an inflammatory bowel disease characterized by inflammatory cell infiltration into the colonic mucosa. e etiology and pathogenesis of ulcerative colitis are not clear [1, 2]. is disorder severely affects the normal life of patients and increases the risk of secondary infections and colon cancer [3]. Ulcerative colitis (UC) is an inflammatory bowel disease characterized by inflammatory cell infiltration into the colonic mucosa. E etiology and pathogenesis of ulcerative colitis are not clear [1, 2]. The exact pathophysiological mechanism of UC is not clear, studies suggest that diet, environment, and intestinal mucosal injury are closely related to the occurrence of UC [6,7,8]. In-depth studies have found that the expression of TJ protein is abnormal in UC, and this directly affects the intestinal mucosal barrier function and plays a key role in promoting the occurrence and development of UC [9]. Erefore, when there is a decrease in TJs, intestinal permeability increases, and this can cause celiac disease, diabetes, UC, and other diseases [10] Intestinal epithelial TJ protein can block the abnormal immune response caused by pathogenic intestinal microorganisms and alleviate the inflammatory response caused by excessive leakage of bacteria and antigens through the mucous membrane [8]. erefore, when there is a decrease in TJs, intestinal permeability increases, and this can cause celiac disease, diabetes, UC, and other diseases [10]
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