Gentiopicroside improves DSS-induced ulcerative colitis and secondary liver injury in mice by enhancing the intestinal barrier and regulating the gut microbiome
Ulcerative colitis (UC) is a chronic inflammatory bowel disease frequently accompanied by intestinal barrier dysfunction and gut microbiome dysbiosis. Emerging evidence suggests that these impairments can contribute to secondary liver injury (SLI) by disrupting the gut–liver axis and promoting hepat...
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| Published in: | Scientific reports Vol. 15; no. 1; pp. 27159 - 16 |
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| Language: | English |
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25.07.2025
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| ISSN: | 2045-2322, 2045-2322 |
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| Abstract | Ulcerative colitis (UC) is a chronic inflammatory bowel disease frequently accompanied by intestinal barrier dysfunction and gut microbiome dysbiosis. Emerging evidence suggests that these impairments can contribute to secondary liver injury (SLI) by disrupting the gut–liver axis and promoting hepatic inflammation. Gentiopicroside (GPS), a natural iridoid glycoside, possesses antimicrobial, anti-inflammatory, and hepatoprotective properties. This study aimed to evaluate the protective effects and underlying mechanisms of GPS in a dextran sulfate sodium (DSS)-induced mouse model of UC and associated SLI. Mice were evaluated for body weight, Disease Activity Index (DAI), colon length, histopathology, tight junction protein expression, gut microbiota composition, inflammatory cytokine levels, and liver function biomarkers. GPS significantly alleviated weight loss, reduced DAI scores, restored intestinal tight junction protein expression, and improved colonic permeability. GPS also modulated the gut microbiota, notably increasing beneficial
Bacteroides
and
Clostridium
cluster IV. Mechanistically, GPS suppressed colonic and hepatic inflammation by inhibiting the TLR4/MyD88/NF-κB and JAK2/STAT3 signaling pathways. Moreover, GPS improved liver function and reduced hepatic inflammatory markers, indicating mitigation of SLI. In conclusion, GPS exerts protective effects against DSS-induced UC and SLI by enhancing intestinal barrier integrity, modulating the gut microbiome, and attenuating inflammation via the gut–liver axis. |
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| AbstractList | Abstract Ulcerative colitis (UC) is a chronic inflammatory bowel disease frequently accompanied by intestinal barrier dysfunction and gut microbiome dysbiosis. Emerging evidence suggests that these impairments can contribute to secondary liver injury (SLI) by disrupting the gut–liver axis and promoting hepatic inflammation. Gentiopicroside (GPS), a natural iridoid glycoside, possesses antimicrobial, anti-inflammatory, and hepatoprotective properties. This study aimed to evaluate the protective effects and underlying mechanisms of GPS in a dextran sulfate sodium (DSS)-induced mouse model of UC and associated SLI. Mice were evaluated for body weight, Disease Activity Index (DAI), colon length, histopathology, tight junction protein expression, gut microbiota composition, inflammatory cytokine levels, and liver function biomarkers. GPS significantly alleviated weight loss, reduced DAI scores, restored intestinal tight junction protein expression, and improved colonic permeability. GPS also modulated the gut microbiota, notably increasing beneficial Bacteroides and Clostridium cluster IV. Mechanistically, GPS suppressed colonic and hepatic inflammation by inhibiting the TLR4/MyD88/NF-κB and JAK2/STAT3 signaling pathways. Moreover, GPS improved liver function and reduced hepatic inflammatory markers, indicating mitigation of SLI. In conclusion, GPS exerts protective effects against DSS-induced UC and SLI by enhancing intestinal barrier integrity, modulating the gut microbiome, and attenuating inflammation via the gut–liver axis. Ulcerative colitis (UC) is a chronic inflammatory bowel disease frequently accompanied by intestinal barrier dysfunction and gut microbiome dysbiosis. Emerging evidence suggests that these impairments can contribute to secondary liver injury (SLI) by disrupting the gut–liver axis and promoting hepatic inflammation. Gentiopicroside (GPS), a natural iridoid glycoside, possesses antimicrobial, anti-inflammatory, and hepatoprotective properties. This study aimed to evaluate the protective effects and underlying mechanisms of GPS in a dextran sulfate sodium (DSS)-induced mouse model of UC and associated SLI. Mice were evaluated for body weight, Disease Activity Index (DAI), colon length, histopathology, tight junction protein expression, gut microbiota composition, inflammatory cytokine levels, and liver function biomarkers. GPS significantly alleviated weight loss, reduced DAI scores, restored intestinal tight junction protein expression, and improved colonic permeability. GPS also modulated the gut microbiota, notably increasing beneficial Bacteroides and Clostridium cluster IV. Mechanistically, GPS suppressed colonic and hepatic inflammation by inhibiting the TLR4/MyD88/NF-κB and JAK2/STAT3 signaling pathways. Moreover, GPS improved liver function and reduced hepatic inflammatory markers, indicating mitigation of SLI. In conclusion, GPS exerts protective effects against DSS-induced UC and SLI by enhancing intestinal barrier integrity, modulating the gut microbiome, and attenuating inflammation via the gut–liver axis. Ulcerative colitis (UC) is a chronic inflammatory bowel disease frequently accompanied by intestinal barrier dysfunction and gut microbiome dysbiosis. Emerging evidence suggests that these impairments can contribute to secondary liver injury (SLI) by disrupting the gut–liver axis and promoting hepatic inflammation. Gentiopicroside (GPS), a natural iridoid glycoside, possesses antimicrobial, anti-inflammatory, and hepatoprotective properties. This study aimed to evaluate the protective effects and underlying mechanisms of GPS in a dextran sulfate sodium (DSS)-induced mouse model of UC and associated SLI. Mice were evaluated for body weight, Disease Activity Index (DAI), colon length, histopathology, tight junction protein expression, gut microbiota composition, inflammatory cytokine levels, and liver function biomarkers. GPS significantly alleviated weight loss, reduced DAI scores, restored intestinal tight junction protein expression, and improved colonic permeability. GPS also modulated the gut microbiota, notably increasing beneficial Bacteroides and Clostridium cluster IV. Mechanistically, GPS suppressed colonic and hepatic inflammation by inhibiting the TLR4/MyD88/NF-κB and JAK2/STAT3 signaling pathways. Moreover, GPS improved liver function and reduced hepatic inflammatory markers, indicating mitigation of SLI. In conclusion, GPS exerts protective effects against DSS-induced UC and SLI by enhancing intestinal barrier integrity, modulating the gut microbiome, and attenuating inflammation via the gut–liver axis. Ulcerative colitis (UC) is a chronic inflammatory bowel disease frequently accompanied by intestinal barrier dysfunction and gut microbiome dysbiosis. Emerging evidence suggests that these impairments can contribute to secondary liver injury (SLI) by disrupting the gut-liver axis and promoting hepatic inflammation. Gentiopicroside (GPS), a natural iridoid glycoside, possesses antimicrobial, anti-inflammatory, and hepatoprotective properties. This study aimed to evaluate the protective effects and underlying mechanisms of GPS in a dextran sulfate sodium (DSS)-induced mouse model of UC and associated SLI. Mice were evaluated for body weight, Disease Activity Index (DAI), colon length, histopathology, tight junction protein expression, gut microbiota composition, inflammatory cytokine levels, and liver function biomarkers. GPS significantly alleviated weight loss, reduced DAI scores, restored intestinal tight junction protein expression, and improved colonic permeability. GPS also modulated the gut microbiota, notably increasing beneficial Bacteroides and Clostridium cluster IV. Mechanistically, GPS suppressed colonic and hepatic inflammation by inhibiting the TLR4/MyD88/NF-κB and JAK2/STAT3 signaling pathways. Moreover, GPS improved liver function and reduced hepatic inflammatory markers, indicating mitigation of SLI. In conclusion, GPS exerts protective effects against DSS-induced UC and SLI by enhancing intestinal barrier integrity, modulating the gut microbiome, and attenuating inflammation via the gut-liver axis.Ulcerative colitis (UC) is a chronic inflammatory bowel disease frequently accompanied by intestinal barrier dysfunction and gut microbiome dysbiosis. Emerging evidence suggests that these impairments can contribute to secondary liver injury (SLI) by disrupting the gut-liver axis and promoting hepatic inflammation. Gentiopicroside (GPS), a natural iridoid glycoside, possesses antimicrobial, anti-inflammatory, and hepatoprotective properties. This study aimed to evaluate the protective effects and underlying mechanisms of GPS in a dextran sulfate sodium (DSS)-induced mouse model of UC and associated SLI. Mice were evaluated for body weight, Disease Activity Index (DAI), colon length, histopathology, tight junction protein expression, gut microbiota composition, inflammatory cytokine levels, and liver function biomarkers. GPS significantly alleviated weight loss, reduced DAI scores, restored intestinal tight junction protein expression, and improved colonic permeability. GPS also modulated the gut microbiota, notably increasing beneficial Bacteroides and Clostridium cluster IV. Mechanistically, GPS suppressed colonic and hepatic inflammation by inhibiting the TLR4/MyD88/NF-κB and JAK2/STAT3 signaling pathways. Moreover, GPS improved liver function and reduced hepatic inflammatory markers, indicating mitigation of SLI. In conclusion, GPS exerts protective effects against DSS-induced UC and SLI by enhancing intestinal barrier integrity, modulating the gut microbiome, and attenuating inflammation via the gut-liver axis. |
| ArticleNumber | 27159 |
| Author | Hu, Xianjing Dai, Weibo Cao, Liu Wang, Yiting Tang, Xiaoqing Niu, Mengyuan |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40715435$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1016_j_phymed_2025_157249 |
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| Keywords | Intestinal barrier Secondary liver injury Gut Microbiome Gentiopicroside Ulcerative colitis |
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| Snippet | Ulcerative colitis (UC) is a chronic inflammatory bowel disease frequently accompanied by intestinal barrier dysfunction and gut microbiome dysbiosis. Emerging... Abstract Ulcerative colitis (UC) is a chronic inflammatory bowel disease frequently accompanied by intestinal barrier dysfunction and gut microbiome dysbiosis.... |
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| SubjectTerms | 692/4020 692/699 Animals Body weight Chemical and Drug Induced Liver Injury - drug therapy Colitis, Ulcerative - chemically induced Colitis, Ulcerative - drug therapy Colitis, Ulcerative - metabolism Colitis, Ulcerative - microbiology Colitis, Ulcerative - pathology Colon Colon - drug effects Colon - pathology Cytokines Dextran Dextran sulfate Dextran Sulfate - adverse effects Diarrhea Digestive system Disease Models, Animal Drug dosages Dysbacteriosis Feces Gastrointestinal Microbiome - drug effects Gastrointestinal tract Gentiopicroside Glycosides Gut Microbiome Gut microbiota Histopathology Humanities and Social Sciences Inflammation Inflammatory bowel disease Inflammatory bowel diseases Intestinal barrier Intestinal microflora Intestinal Mucosa - drug effects Intestinal Mucosa - metabolism Intestine Iridoid Glucosides - pharmacology Iridoid Glucosides - therapeutic use Janus kinase 2 Kinases Laboratory animals Liver Liver - drug effects Liver - metabolism Liver - pathology Male Mice Mice, Inbred C57BL Microbiomes Microbiota Molecular weight multidisciplinary MyD88 protein NF-κB protein Phosphatase Protease inhibitors Protein composition Science Science (multidisciplinary) Secondary liver injury Signal Transduction - drug effects Stat3 protein TLR4 protein Toll-Like Receptor 4 - metabolism Toll-like receptors Traditional Chinese medicine Tumor necrosis factor-TNF Ulcerative colitis |
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| Title | Gentiopicroside improves DSS-induced ulcerative colitis and secondary liver injury in mice by enhancing the intestinal barrier and regulating the gut microbiome |
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