文献类型：期刊文献

英文题名：Therapeutic potential of Qihuang Biwen Formula and its bioactive compounds for the treatment of ulcerative colitis in Drosophila and mice

作者：Wang, Huinan[1,2];Xiu, Minghui[1];Zhou, Shihong[1];Zhang, Yongxuan[1];Fu, Jinyu[1];Jiang, Xiaolin[1];Zhao, Bing[1];Liu, Yongqi[1];Zhang, Zhiming[3];He, Jianzheng[1,4]

第一作者：Wang, Huinan

通信作者：Liu, YQ[1];He, JZ[1];Zhang, ZM[2];He, JZ[3]

机构：[1]Gansu Univ Chinese Med, Lanzhou 730000, Peoples R China;[2]Second Hosp Gansu Prov, Lanzhou 730000, Peoples R China;[3]Gansu Prov Hosp Tradit Chinese Med, Lanzhou 730000, Peoples R China;[4]Res Ctr Tradit Chinese Med, Lanzhou 730000, Gansu, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Lanzhou 730000, Peoples R China;[2]corresponding author), Gansu Prov Hosp Tradit Chinese Med, Lanzhou 730000, Peoples R China;[3]corresponding author), Res Ctr Tradit Chinese Med, Lanzhou 730000, Gansu, Peoples R China.|[10735]甘肃中医药大学;

年份：2026

卷号：155

外文期刊名：PHYTOMEDICINE

收录：;Scopus(收录号：2-s2.0-105033582849);WOS:【SCI-EXPANDED(收录号:WOS:001728352600001)】；

基金：This work was supported by the Major Science and Technology Projects in Gansu Province (No.22ZD1FA001) , Gansu Natural Science Foundation (No. 25JRRA833) , Development Project of Gansu Provincial Traditional Chinese Medicine Research Center (No. zyzx-2024-zx18) , Foundation from Key Laboratory of Dunhuang Medicine (No. DHYX24-02) .

语种：英文

外文关键词：Qihuang Biwen Formula; Ulcerative colitis; TLR4/NF-kappa B signaling pathway; Oxidative phosphorylation; Bioactive compounds

摘要：Background: Qihuang Biwen Formula (QHBWF), derived from the classic Yupingfeng Powder, is traditionally used for immune regulation. While clinically applied, its mechanism of action in ulcerative colitis (UC) remains unclear. Purpose: The effectiveness and underlying principles of QHBWF for UC treatment were investigated using both Drosophila and mice models, and its bioactive components were identified. Methods: In the dextran sulfate sodium (DSS)-induced adult fly, the survival rate, locomotion, excretion, smurf, digestive capacity, intestinal length, death of intestinal epithelial cells (IECs), and proliferation of intestinal stem cells (ISCs) were measured. Meanwhile, the body weight, intestinal length, disease activity index, histopathology, serum cytokine levels, and ROS levels were detected in the UC mouse. Additionally, the mechanism of QHBWF was investigated by bioinformatics analysis, transcriptomic analysis, qRT-PCR, immunohistochemistry and western blotting (WB). Finally, UCPL-MS/MS technology and phenotype assays in UC flies were used to screen the key bioactive components of QHBWF. Results: QHBWF significantly improved survival rate, locomotor activity, and intestinal function. It restored intestinal morphology, suppressed aberrant intestinal stem cell (ISC) proliferation, and reduced intestinal epithelial cell (IEC) apoptosis in DSS treated flies. In mice, QHBWF alleviated weight loss, colon shortening, and DAI scores, improved histopathology, and reduced IL-6, IL-1 beta, and intestinal ROS. These results indicated that QHBWF could alleviate the intestinal injury in both UC models. Mechanistically, QHBWF down-regulated mRNA levels of Toll signaling and the Imd signaling, and up-regulated the gene expression of mitochondrial oxidative phosphorylation (OXPHOS) complexes in the intestines of UC flies. Consistently, QHBWF decreased the protein levels of TLR4, MyD88 and NF-kappa B p65, and promoted the protein expresses of NDUFB8, SDHB and ATP5A in the guts of UC mice. These indicated that QHBWF inhibited the TLR4/NF-kappa B signaling pathway and activated the OXPHOS function. Furthermore, kaempferol, emodin, quercetin, isochlorogenic acid, and chlorogenic acid could extend the survival rate, increased the intestinal length, and facilitated intestinal barrier repair in UC flies. Conclusion: QHBWF exerted anti-colitis effects by regulating immunity and metabolism, targeting the TLR4/NF kappa B signaling pathway and mitochondrial oxidative phosphorylation. Kaempferol, emodin, quercetin, isochlorogenic acid, and chlorogenic acid were the bioactive compounds of QHBWF against UC. This study provides the potential of QHBWF as a multi-target treatment for UC.