Dunhuang Gancao Fuling Xingren decoction and its components alleviate CPT-11 induced intestinal mucositis

Sep 29, 2026

Dunhuang Gancao Fuling Xingren decoction (GFXD), a traditional formulation from the Dunhuang Ancient Medical Prescriptions, is investigated for its ability to protect against irinotecan (CPT-11)-induced intestinal mucositis (CIM). Therapeutic efficacy and mechanisms are examined in Drosophila and C57BL/6 J mice using histology, staining, cytokine assays, transcriptomics, 16S rRNA sequencing, FMT, antibiotics, and LC–MS. Results indicate GFXD improves survival and gut integrity, restores inflammatory balance, modulates gut microbiota, and suppresses Toll-Imd and JAK-STAT signaling, with formononetin, kaempferol, and ergosterol as key bioactive compounds.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages22

Reading Time55 min

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Abstract

Background

Purpose

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Wu et al. Chinese Medicine (2026) 21:4 [https://doi.org/10.1186/s13020-025-01279-8](https://doi.org/10.1186/s13020-025-01279-8) Chinese Medicine RESEARCH Open Access Dunhuang Gancao Fuling Xingren decoction and its components alleviate CPT-11 induced intestinal mucositis by regulating gut microbiota related innate immunity and inflammatory response in Drosophila and mice Jinhan Wu1†, Minghui Xiu2,3†, Xiaoqian Wang1, Peihao Zhang1, Yujie Qin2, Jiangnan Li1, Xiaolin Jiang1, Yaoxing Duan4, Yongqi Liu1,3* and Jianzheng He 1,4,5* Abstract Background Dunhuang Gancao Fuling Xingren decoction (GFXD) is a traditional formulation derived from the Dunhuang Ancient Medical Prescriptions, has been historically utilized for its immunomodulatory and anti-inflammatory properties. However, the protective effect against irinotecan (CPT-11)-induced intestinal mucositis (CIM) remains poorly elucidated. Purpose To investigate the therapeutic efficacy of GFXD in alleviating CIM and elucidate its underlying mechanism and components using Drosophila melanogaster and C57BL/6 J mouse models. Methods The therapeutic efficacy of GFXD was assessed in both Drosophila and mouse models by phenotype assay, hematoxylin and eosin (H&E) staining, and Alcian blue-periodic acid schiff (AB-PAS) staining. Transcriptomic profiling combined with 16S rRNA sequencing were employed to identify potential mechanisms of GFXD regulating CPT-11-induced mucositis. Cytokine levels were measured using ELISA, while the expression levels of key signaling pathways, including Toll-Imd and JAK-STAT pathways were analyzed via qRT-PCR, immunofluorescence, fecal microbiota transplantation (FMT) experiment, and antibiotic treatment. Furthermore, functional components of GFXD were characterized via liquid chromatography-mass spectrometry (LC–MS), and their efficacy was validated in CPT-11-treated Drosophila. Results GFXD significantly mitigated CPT-11-induced systemic and intestinal damage in Drosophila, evidenced by improved survival rate, restored digestive function, elongated intestinal length, reduced acid–base imbalance, and enhanced epithelial and stem cell proliferation. In mice, GFXD alleviated mucositis symptoms, attenuated histopathological damage, and normalized inflammatory cytokine levels. Mechanistically, GFXD suppressed gut microbiota †Jinhan Wu and Minghui Xiu have contributed equally to this work. *Correspondence: Yongqi Liu [liuyongqi73@163.com](liuyongqi73@163.com)[ ](liuyongqi73@163.com)Jianzheng He[hejianzheng1006@163.com](hejianzheng1006@163.com) Full list of author information is available at the end of the article © The Author(s) 2026. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creativecommons.org/licenses/by/4.0/](http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ()[. The Creative Commons Public Domain Dedication waiver (](http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ()[http://creativeco](http://creativeco)[mmons.org/publicdomain/zero/1.0/](mmons.org/publicdomain/zero/1.0/)) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

FAQs

What condition does the study target?

The study targets chemotherapy-induced intestinal mucositis (CIM) caused by irinotecan (CPT-11). It evaluates whether GFXD can alleviate intestinal damage and related inflammatory changes.

How was GFXD evaluated in the experiments?

GFXD efficacy was assessed in Drosophila and mouse models using phenotype assays, H&E and AB-PAS staining, cytokine measurements by ELISA, pathway expression analysis via qRT-PCR and immunofluorescence, and microbiota interventions including FMT and antibiotic treatment.

What mechanism does the study propose for GFXD’s protective effect?

GFXD is proposed to alleviate CIM by modulating gut microbiota composition, enriching beneficial microbes and reducing pathogens, and suppressing hyperactivation of Toll-Imd and JAK-STAT immune signaling pathways.

Which compounds are identified as active components of GFXD?

Formononetin, kaempferol, and ergosterol are identified as functional components. Their efficacy was validated in CPT-11-treated Drosophila, supporting their role in mitigating intestinal injury.

Sep 29, 2026

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