Frontiers in pharmacology · 2026
Clinodiside A, an active metabolite in Clinopodii herba, alleviates dextran-sulfate-sodium-induced ulcerative colitis.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Yang Xingxing, Fan Yujia, Lin Qiong, Ni Jinxin, Tan Xinsheng, Xu Jiajun, Sun Min
Аннотация
INTRODUCTION: Clinodiside A is a natural bioactive component of Clinopodii herba, a genuine regional herb from Anhui Province (China) with multiple biological activities. This study aimed to explore the therapeutic potential of Clinodiside A in ulcerative colitis (UC).
METHODS: Dextran sulfate sodium (DSS) was used to establish UC models both in vivo and in vitro. The models were treated with Clinodiside A. Parameters including body weight, disease activity index (DAI) score, colon length, and inflammation were assessed. Iron overload, lipid peroxidation, and intestinal epithelial repair were also evaluated. In vitro experiments using HCT116 cells examined cell damage, motility, and recovery.
RESULTS: Clinodiside A alleviated DSS-induced UC consequences, including weight loss, increased DAI score, colon shortening, and inflammation. These effects were associated with reduced iron overload, reduced lipid peroxidation, and enhanced intestinal epithelial repair. In HCT116 cells, Clinodiside A ameliorated damage, enhanced motility, and promoted recovery of the intestinal epithelium.
DISCUSSION: Our research validates the therapeutic and protective effects of Clinodiside A from Clinopodii herba on UC and expands its application potential.
METHODS: Dextran sulfate sodium (DSS) was used to establish UC models both in vivo and in vitro. The models were treated with Clinodiside A. Parameters including body weight, disease activity index (DAI) score, colon length, and inflammation were assessed. Iron overload, lipid peroxidation, and intestinal epithelial repair were also evaluated. In vitro experiments using HCT116 cells examined cell damage, motility, and recovery.
RESULTS: Clinodiside A alleviated DSS-induced UC consequences, including weight loss, increased DAI score, colon shortening, and inflammation. These effects were associated with reduced iron overload, reduced lipid peroxidation, and enhanced intestinal epithelial repair. In HCT116 cells, Clinodiside A ameliorated damage, enhanced motility, and promoted recovery of the intestinal epithelium.
DISCUSSION: Our research validates the therapeutic and protective effects of Clinodiside A from Clinopodii herba on UC and expands its application potential.