Abstract
Background and Aims Intestinal fibrosis is one of the severe and common complications of Crohn's disease (CD), but the etiology and pathogenesis remain uncertain. The study intended to examine whether the effect of herb-partitioned moxibustion on rats with CD-associated intestinal fibrosis is associated with the RhoA/ROCK1/MLC pathway. Methods All experimental rats were randomly allocated into the normal control group (NC), model control group (MC), and herb-partitioned moxibustion group (HPM). Intestinal fibrosis was established in rats with CD by repeated rectal administrations of 2,4,6-trinitrobenzenesulfonic acid (TNBS). Herb-partitioned moxibustion was applied at the Qihai (CV6) and Tianshu (ST25) acupoints once daily for 10 days in the HPM group. In this study, histological changes were examined by hematoxylin and eosin (HE) staining; then, Masson's trichrome staining was used to assess the degree of fibrosis in each group. Experimental methods of immunohistochemistry, western blotting, and real-time PCR were applied to detect the levels of α-SMA, collagen III, RhoA, ROCK1, and p-MLC. Moreover, the double immunofluorescent staining for the colocalization of both α-SMA and ROCK1 was performed. Results Contrasted with the normal controls, the collagen deposition and fibrosis scores were increased in colonic tissue of model rats, and HPM decreased the collagen deposition and fibrosis scores. The protein of α-SMA and collagen III in the MC group exceeds that of the NC group; HPM decreased the expression of α-SMA and collagen III in rats with intestinal fibrosis. Similarly, the expression of RhoA, ROCK1, and p-MLC in model rats was obviously increased compared with normal controls; the expression of RhoA, ROCK1, and p-MLC was decreased after HPM. The coexpression of α-SMA and ROCK1 in rats with intestinal fibrosis was higher than normal rats. Conclusion HPM improves CD-associated intestinal fibrosis by suppressing the RhoA/ROCK1/MLC pathway.
Highlights
Intestinal fibrosis is one of the severe and common complications of Crohn’s disease (CD), which can invade almost all parts of the digestive tract and involve the entire intestinal wall, with abdominal pain, constipation, lumen narrowing, and even intestinal obstruction or intestinal perforation [1]
2,4,6-trinitrobenzenesulfonic acid (TNBS) was used to establish the model of CD-associated intestinal fibrosis. e degree of intestinal fibrosis was examined by histopathology; the level of α-SMA, collagen III, ROCK1, RhoA, and p-MLC was measured to elucidate the mechanism through immunohistochemistry, western blotting, and real-time PCR, by which herb-partitioned moxibustion group (HPM) affects CD-associated intestinal fibrosis
Fissured ulcers were present, fibrous tissue had proliferated around the ulcer, and a large amount of granulated tissue had formed in the mucosa, submucosa, and muscle, accompanied by abundant infiltrated fibroblasts. ere are healing ulcers in the mucosal layer covered with new epithelial cells in the HPM group; some glands were irregular or had disappeared, with a small inflammatory cell infiltration and fibroblast proliferation (Figure 1)
Summary
Intestinal fibrosis is one of the severe and common complications of Crohn’s disease (CD), which can invade almost all parts of the digestive tract and involve the entire intestinal wall, with abdominal pain, constipation, lumen narrowing, and even intestinal obstruction or intestinal perforation [1]. E RhoA/ROCK1 pathway plays a vital role in cytoskeletal remodeling and regulates fundamental cellular processes, including cell motility, contraction, adhesion, and proliferation [7, 8]. A preclinical study showed that ROCK was activated in intestinal fibroblasts, epithelial cells, endothelial cells, and muscle cells in patients with CD-associated intestinal fibrosis [11]. Erefore, we hypothesize that the RhoA/ROCK1/ MLC pathway may take part in the pathological process of intestinal fibrosis. The common treatment about CD-associated intestinal fibrosis only focuses on anti-inflammatory rather than antifibrosis; the use of biological agents does not significantly alleviate this disease [15]. E degree of intestinal fibrosis was examined by histopathology; the level of α-SMA, collagen III, ROCK1, RhoA, and p-MLC was measured to elucidate the mechanism through immunohistochemistry, western blotting, and real-time PCR, by which HPM affects CD-associated intestinal fibrosis 2,4,6-trinitrobenzenesulfonic acid (TNBS) was used to establish the model of CD-associated intestinal fibrosis. e degree of intestinal fibrosis was examined by histopathology; the level of α-SMA, collagen III, ROCK1, RhoA, and p-MLC was measured to elucidate the mechanism through immunohistochemistry, western blotting, and real-time PCR, by which HPM affects CD-associated intestinal fibrosis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Evidence-Based Complementary and Alternative Medicine
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
