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Multi-Omics-Driven Network Pharmacology and Experimental Validation Reveal the Molecular Mechanism of Bupi Yichang Pill in Treating Ulcerative Colitis Through Regulation of the PI3K/Akt/IKK/NF-κB Pathway.
Journal of ethnopharmacology

Cure8 research brief

Multi-Omics-Driven Network Pharmacology and Experimental Validation Reveal the Molecular Mechanism of Bupi Yichang Pill in Treating Ulcerative Colitis Through Regulation of the PI3K/Akt/IKK/NF-κB Pathway.

2 min read

Why This Matters

This study explores a multi-component traditional medicine that the authors report can reduce experimental colitis and modulate inflammatory signaling and the gut microbiome — findings that could guide future preclinical work and identification of bioactive compounds relevant to UC therapies.

Who Should Pay Attention

Researchers studying IBD mechanisms, microbiome–host interactions, and natural-product drug discovery; clinicians interested in emerging preclinical evidence about complementary therapies; patients curious about laboratory research on traditional medicines (not clinical recommendations).

Study Snapshot

Story typeResearch paper
Evidence typeResearch paper
Source depthJournal abstract

What To Know

This paper reports an experimental study using a DSS-induced mouse model of ulcerative colitis to evaluate a traditional Chinese medicine formula, Bupi Yichang Pill (BYP).

The authors combined chemical profiling (UHPLC-HRMS), network pharmacology, multi-omics (16S rRNA sequencing, untargeted metabolomics, RNA‑seq), molecular docking, and laboratory validation (Western blot, immunofluorescence, ELISA, RT‑qPCR) to investigate mechanisms.

They identify multiple candidate bioactive compounds (e.g., kaempferol, liquiritin, quercetin, berberine) and implicate suppression of the PI3K/Akt/IKK/NF-κB signaling axis alongside changes in gut microbiota and metabolism as possible mechanisms.

The study includes biochemical and histologic readouts showing BYP limited DSS-colitis severity in mice (body weight, DAI, colon length, mucosal injury) and altered inflammatory cytokine profiles (TNF-α, IL-1β, IL-6 down; IL-10 up).

Multi-omics results are reported to show shifts in microbial composition and metabolic pathways (bile acid and amino acid metabolism), and western blots/immunofluorescence supported reduced phosphorylation of PI3K, Akt, IKK, and NF-κB p65 in colon tissue and LPS‑stimulated macrophages.

This brief is grounded in the article abstract and reported experimental methods; Cure8 has not reviewed the full paper beyond the supplied abstract and extracted text.

Keep In Mind

Preclinical mouse models and multi-omics analyses can suggest mechanisms and candidate compounds but do not establish safety or efficacy in humans. The results are experimental and hypothesis-generating; clinical trials would be required before any treatment recommendations.

The summary is based on the article abstract/extracted text provided, not an independent full-text peer review.

Source Details

Review the original publication for the complete reporting, methods, and context.

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Research paper Evidence type derived from source or registry metadata.
PublicationJournal of ethnopharmacology
AuthorsYunlu Zou, Zidong Yang, Jiatong Liu +3 more
InstitutionCollege of Pharmacy, Changchun University of Chinese Medicine, Changchun, Jilin, China.
Study typeJournal article
Indexed viaPubMed
Source typeResearch paper
PublishedAug 8, 2026, 12:00 AM
Content availableJournal abstract

Conflict statement: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

This Cure8 brief is based on source text from the linked article. Cure8 is informational only and is not a substitute for professional medical advice, diagnosis, or treatment.

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