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Main Article Content
Tong-Xie-Yao-Fang improves chronic intestinal fibrosis in mice with colitis through CRH-R2-mediated IL-6/STAT3 signaling pathway
Abstract
Purpose: To investigate the potential mechanism of action of Tong-Xie-Yao-Fang (TXYF) on
inflammation-related intestinal fibrosis in mice. In addition, to examine dextran sodium sulfate (DSS)
induction and the stimulation of human intestinal fibroblasts (CCD-18Co) by transforming growth factor-
β1 (TGF-β1).
Methods: Chronic colitis in C57BL/6 mice was induced by administering 2 % DSS and TXYF extract
(11.2 g/kg per day). An intestinal fibrosis cell model was constructed by stimulating CCD-18Co cells with
TGF-β1 (10 ng/mL). The status and weight loss of colitis of the mice was assessed by Disease Activity
Index (DAI) while colonic tissue injury and fibrosis were assessed using hematoxylin-eosin (H&E)
staining and Masson’s trichrome staining. Relative expression levels of corticotrophin-releasing
hormone receptor 2 (CRH-R2) and Interleukin 6 (IL-6)/signal transducer and activator of transcription 3
(STAT3) in colon tissues and CCD-18Co cells were determined using Western blot. A cell model of
intestinal fibrosis was constructed by stimulating CCD-18Co cells with TGF-β1 (10 ng/mL). At the same
time, the cells were subjected to the intervention of TXYF drug-containing serum (TXYF-DS).
Results: TXYF significantly improve the pathological changes, weight loss, and DAI score of colon
tissue in DSS induced colitis mice (p < 0.05). The expression levels of IL-6 and p-STAT3 were
significantly reduced, while the expression level of CRH-R2 was upregulated in the mouse colon tissue
(p < 0.05). At the cellular level, TXYF-DS intervention significantly reduced cell mortality and mitigated
the degree of cell fibrosis (p < 0.05). Furthermore, the expression level of CRH-R2 was up-regulated
while that of IL-6 and p-STAT3 were down-regulated.
Conclusion: TXYF ameliorates chronic intestinal fibrosis in colitis-afflicted mice by restricting IL-
6/STAT3 signaling pathway whilst upregulating CRH-R2 expression.
