Hongyuyin attenuates intestinal fibrosis in ulcerative colitis in mice revealed by transcriptomic and network pharmacology analyses

Abstract Ulcerative colitis (UC) is a chronic, idiopathic inflammatory disease affecting the gastrointestinal tract. Hongyuyin (HYY), a traditional Chinese botanical formulation, has been effectively treating UC for over three decades; however, its underlying biological mechanism of action in UC-ass...

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Main Authors: Qin Qin, Qingjun Dong, Yan Pan, Chen Wang, Jingen Lu
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-06021-w
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author Qin Qin
Qingjun Dong
Yan Pan
Chen Wang
Jingen Lu
author_facet Qin Qin
Qingjun Dong
Yan Pan
Chen Wang
Jingen Lu
author_sort Qin Qin
collection DOAJ
description Abstract Ulcerative colitis (UC) is a chronic, idiopathic inflammatory disease affecting the gastrointestinal tract. Hongyuyin (HYY), a traditional Chinese botanical formulation, has been effectively treating UC for over three decades; however, its underlying biological mechanism of action in UC-associated intestinal fibrosis (IF) remains unclear. This study investigated the mechanisms of action of HYY on IF through in vivo experiments using a dextran sulfate sodium (DSS)-induced mouse colitis model. Clinical symptoms, colonic pathological damage, inflammation, and fibrosis were monitored across all groups. Both transcriptomic analysis and network pharmacology (NP) techniques were utilized to elucidate the mechanistic insights. HYY treatment substantially reduced inflammation, fibroblast activation, and collagen deposition in UC mice. KEGG analyses suggested that HYY treatment modulated multiple signaling pathways, notably the TNF, IL-17, and PI3K-Akt signaling pathways. Combined analysis identified the PI3K-Akt signaling pathway as a major contributor, with high enrichment factors and numerous enrichment genes involved (IL-6, CSF3, SPP1, AKT1, PIK3CA, and so on) in UC-associated IF. Western blotting confirmed significant reductions in both p-AKT/AKT and p-mTOR/mTOR ratios after HYY treatment. Collectively, HYY alleviates UC-associated IF by reducing the phosphorylation of PI3K-Akt pathway factors, thereby inhibiting fibroblast activation and collagen deposition. This research provides novel insights into HYY’s mechanism of action in UC-associated IF management.
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spelling doaj-art-172fda35403546c7b6e427a3dd393fcd2025-08-20T04:01:34ZengNature PortfolioScientific Reports2045-23222025-07-0115111810.1038/s41598-025-06021-wHongyuyin attenuates intestinal fibrosis in ulcerative colitis in mice revealed by transcriptomic and network pharmacology analysesQin Qin0Qingjun Dong1Yan Pan2Chen Wang3Jingen Lu4Institute of Chinese Traditional Surgery, Longhua Hospital, Shanghai University of Traditional Chinese MedicineDepartment of Anal & Intestinal Disease, Longhua Hospital, Shanghai University of Traditional Chinese MedicineDepartment of Anal & Intestinal Disease, Longhua Hospital, Shanghai University of Traditional Chinese MedicineDepartment of Anal & Intestinal Disease, Longhua Hospital, Shanghai University of Traditional Chinese MedicineDepartment of Anal & Intestinal Disease, Longhua Hospital, Shanghai University of Traditional Chinese MedicineAbstract Ulcerative colitis (UC) is a chronic, idiopathic inflammatory disease affecting the gastrointestinal tract. Hongyuyin (HYY), a traditional Chinese botanical formulation, has been effectively treating UC for over three decades; however, its underlying biological mechanism of action in UC-associated intestinal fibrosis (IF) remains unclear. This study investigated the mechanisms of action of HYY on IF through in vivo experiments using a dextran sulfate sodium (DSS)-induced mouse colitis model. Clinical symptoms, colonic pathological damage, inflammation, and fibrosis were monitored across all groups. Both transcriptomic analysis and network pharmacology (NP) techniques were utilized to elucidate the mechanistic insights. HYY treatment substantially reduced inflammation, fibroblast activation, and collagen deposition in UC mice. KEGG analyses suggested that HYY treatment modulated multiple signaling pathways, notably the TNF, IL-17, and PI3K-Akt signaling pathways. Combined analysis identified the PI3K-Akt signaling pathway as a major contributor, with high enrichment factors and numerous enrichment genes involved (IL-6, CSF3, SPP1, AKT1, PIK3CA, and so on) in UC-associated IF. Western blotting confirmed significant reductions in both p-AKT/AKT and p-mTOR/mTOR ratios after HYY treatment. Collectively, HYY alleviates UC-associated IF by reducing the phosphorylation of PI3K-Akt pathway factors, thereby inhibiting fibroblast activation and collagen deposition. This research provides novel insights into HYY’s mechanism of action in UC-associated IF management.https://doi.org/10.1038/s41598-025-06021-wUlcerative colitisIntestinal fibrosisPI3KAKTTranscriptomicsNetwork pharmacology
spellingShingle Qin Qin
Qingjun Dong
Yan Pan
Chen Wang
Jingen Lu
Hongyuyin attenuates intestinal fibrosis in ulcerative colitis in mice revealed by transcriptomic and network pharmacology analyses
Scientific Reports
Ulcerative colitis
Intestinal fibrosis
PI3K
AKT
Transcriptomics
Network pharmacology
title Hongyuyin attenuates intestinal fibrosis in ulcerative colitis in mice revealed by transcriptomic and network pharmacology analyses
title_full Hongyuyin attenuates intestinal fibrosis in ulcerative colitis in mice revealed by transcriptomic and network pharmacology analyses
title_fullStr Hongyuyin attenuates intestinal fibrosis in ulcerative colitis in mice revealed by transcriptomic and network pharmacology analyses
title_full_unstemmed Hongyuyin attenuates intestinal fibrosis in ulcerative colitis in mice revealed by transcriptomic and network pharmacology analyses
title_short Hongyuyin attenuates intestinal fibrosis in ulcerative colitis in mice revealed by transcriptomic and network pharmacology analyses
title_sort hongyuyin attenuates intestinal fibrosis in ulcerative colitis in mice revealed by transcriptomic and network pharmacology analyses
topic Ulcerative colitis
Intestinal fibrosis
PI3K
AKT
Transcriptomics
Network pharmacology
url https://doi.org/10.1038/s41598-025-06021-w
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AT yanpan hongyuyinattenuatesintestinalfibrosisinulcerativecolitisinmicerevealedbytranscriptomicandnetworkpharmacologyanalyses
AT chenwang hongyuyinattenuatesintestinalfibrosisinulcerativecolitisinmicerevealedbytranscriptomicandnetworkpharmacologyanalyses
AT jingenlu hongyuyinattenuatesintestinalfibrosisinulcerativecolitisinmicerevealedbytranscriptomicandnetworkpharmacologyanalyses