文献类型：期刊文献

英文题名：Caffeic Acid Protects Against Ulcerative Colitis via Inhibiting Mitochondrial Apoptosis and Immune Overactivation in Drosophila

作者：Xiu, Minghui[1,2];Li, Botong[3];He, Li[1];Shi, Yan[3];Zhang, Yongxuan[1];Zhou, Shihong[1];Liu, Yongqi[2,3];Wang, Ningbo[4];He, Jianzheng[2,3,5]

第一作者：修明慧;Xiu, Minghui

通信作者：He, JZ[1];He, JZ[2];He, JZ[3]

机构：[1]Gansu Univ Chinese Med, Coll Publ Hlth, Lanzhou City, Gansu Province, Peoples R China;[2]Minist Educ, Key Lab Dunhuang Med, Lanzhou City, Gansu Province, Peoples R China;[3]Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Prevent & T, Tradit Chinese Med Res Gansu Coll & Univ, Lanzhou City, Gansu Province, Peoples R China;[4]Qinghai Univ, Tibetan Med Coll, Xining City, Qinghai Provinc, Peoples R China;[5]Gansu Univ Chinese Med, Res & Expt Ctr, Lanzhou City, Gansu Province, Peoples R China

第一机构：甘肃中医药大学公共卫生学院

通信机构：[1]corresponding author), Minist Educ, Key Lab Dunhuang Med, Lanzhou City, Gansu Province, Peoples R China;[2]corresponding author), Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Prevent & T, Tradit Chinese Med Res Gansu Coll & Univ, Lanzhou City, Gansu Province, Peoples R China;[3]corresponding author), Gansu Univ Chinese Med, Res & Expt Ctr, Lanzhou City, Gansu Province, Peoples R China.|[10735]甘肃中医药大学;

年份：2025

卷号：19

起止页码：2157

外文期刊名：DRUG DESIGN DEVELOPMENT AND THERAPY

收录：;Scopus(收录号：2-s2.0-105001444916);WOS:【SCI-EXPANDED(收录号:WOS:001450718000001)】；

基金：Funding This work was supported by the National Natural Science Foundation of China (No. 82360896) , Gansu Provincial Department of Education Innovation Ability Enhancement Project (No. 2023A-086) , Lanzhou Science and Technology Plan Project (No. 2023-4-53) , and the Foundation of Key Laboratory of Dunhuang Medicine (No. DHYX21-05) .

语种：英文

外文关键词：ulcerative colitis; caffeic acid; toll and Imd pathways; apoptosis; Drosophila melanogaster

摘要：Background: Ulcerative colitis (UC) is a chronic intestinal inflammation that is prone to relapse and is difficult to fully recover; therefore, there is a need for safer alternative treatments. Caffeic acid (CA) is a natural polyphenolic compound that has antioxidant and anti-inflammatory properties. However, the beneficial effects and mechanisms of action of CA in UC remain unclear. Purpose: This study evaluated the protective effect of CA against dextran sulfate sodium (DSS)-induced intestinal injury in Drosophila melanogaster model. Results: Oral administration of CA significantly reduced body damage in UC flies, improved their survival rate, restored damaged digestion, and improved locomotion. CA supplementation significantly alleviated intestinal damage in UC flies by restoring excretion balance, repairing intestinal atrophy, improving acid-base balance imbalance, inhibiting intestinal structural destruction, inhibiting intestinal epithelial cell death and intestinal stem cell (ISC) excessive proliferation, and reducing the number of harmful bacteria. Mechanistic studies found that CA significantly reduced the expression of Toll and Imd pathway genes (including Myd88, Dif, PGRP-LC, Imd, Rel, and Dpt), reduced ROS levels and the expression of apoptosis-related genes (Debcl, Cyt-c-p, DrlCE, Dronc, and Dark), and increased ATP and MFN2 levels. Conclusion: CA alleviated intestinal damage mainly by inhibiting the Toll and Imd signaling pathways and inhibiting apoptosis mediated by mitochondrial damage. These findings suggest that CA holds promise as a potential therapeutic for UC treatment.