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

Abstract

AbstractBackgroundUlcerative 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.MethodsThis 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.ResultsNeither 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.ConclusionsThis 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.