Investigation of Ogikenchuto (TJ-98) for intestinal fibrosis using a mouse model of dextran sulfate sodium-induced colitis

Background: Ulcerative colitis (UC) is a chronic inflammatory disease of unknown etiology. Although various new drugs have been developed in recent years, many of them are expensive, generating a demand for inexpensive and useful therapeutic drugs. Ogikenchuto (TJ-98), an existing Kampo medicine, has been used to treat ulcers and similar conditions for some time. The current study therefore investigated whether TJ-98 could be a new therapeutic agent for UC, a chronic inflammatory disease. Methods: This study used 6-week-old female C57BL/6J mice to establish a mouse model of dextran sulfate sodium (DSS)-induced colitis. We then evaluated the therapeutic effects of tacrolimus and TJ-98 on colitis based on body weight, intestinal length, intestinal fibrosis, and cytokines. Sirius red staining was used to evaluate intestinal fibrosis, while interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were used to evaluate cytokines involved in inflammation. Results: Neither tacrolimus nor TJ-98 ameliorated weight loss. Although tacrolimus did not remediate intestinal shortening, intestinal fibrosis, or cytokine levels (IL-1β, IL-6, and TNF-α), TJ-98 did ameliorate intestinal shortening and intestinal fibrosis and decrease IL-1β levels. Conclusions: This study confirmed that TJ-98 suppressed the inflammation caused by DSS-induced enteritis and decreased the associated intestinal fibrosis, highlighting its potential as an inexpensive novel therapeutic agent for UC.