Background and aims: Intestinal fibrosis is one of the severe and common complications of Crohn’s disease, but the etiology and pathogenesis remain uncertain. The study intended to examine whether the effect of herb-partitioned moxibustion on rats with Crohn’s disease-associated intestinal fibrosis is associated with the RhoA/ROCK1/MLC pathway.
Methods: All experimental rats were randomly allocated into the normal control group, model control group, and herb-partitioned moxibustion group. Intestinal fibrosis was established in rats with Crohn’s disease 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 herb-partitioned moxibustion group decreased the collagen deposition and fibrosis scores. The protein of α-SMA and collagen III in the model control group group exceeds that of the normal control group group; herb-partitioned moxibustion group 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 herb-partitioned moxibustion group. The coexpression of α-SMA and ROCK1 in rats with intestinal fibrosis was higher than normal rats.
Conclusion: Herb-partitioned moxibustion group improves Crohn’s disease-associated intestinal fibrosis by suppressing the RhoA/ROCK1/MLC pathway.