ArticleEvidence-based complementary and alternative medicine : eCAM2022
Mechanism of Fructus Mume Pills Underlying Their Protective Effects in Rats with Acetic Acid-Inducedulcerative Colitis via the Regulation of Inflammatory Cytokines and the VEGF-PI3K/Akt-eNOS Signaling Pathway.
Article in Evidence-based complementary and alternative medicine : eCAM, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Evaluation ofFood science & nutrition · 2025Article
- Protective effect of Dulaglutide, a GLP1 agonist, on acetic acid-induced ulcerative colitis in rats: involvement of GLP-1, TFF-3, and TGF-β/PI3K/NF-κB signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Physiologically-Modeled Dynamic Stimulation and Growth Factors Induce Differentiation of Mesenchymal Stem Cells to a Vascular Endothelial Cell Phenotype.Microcirculation (New York, N.Y. : 1994) · 2025Article
- Targeting the PI3K/Akt pathway for the treatment of ulcerative colitis: integrative regulatory features of traditional Chinese medicine.Frontiers in pharmacology · 2025Review
- Evaluation of the Mechanism of Sinomenii Caulis in Treating Ulcerative Colitis based on Network Pharmacology and Molecular Docking.Current computer-aided drug design · 2024Article
- Protective Application of Chinese Herbal Compounds and Formulae in Intestinal Inflammation in Humans and Animals.Molecules (Basel, Switzerland) · 2023Review
- Effect of DietaryAnimals : an open access journal from MDPI · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Fructus mume pills (FMPs) have been clinically proven to be effective for treating ulcerative colitis (UC). However, the therapeutic and protective mechanisms have not been fully studied. Aim: We aimed to explore the mechanism of FMPs in an acetic acid (AA)-induced ulcerative colitis rat model. Methods: The targets, GO terms, and KEGG pathways for the FMPs and UC were screened and constructed using network pharmacology. A possible mechanism was verified in a 4% AA-induced colitis rat model. Colitis activity and state were evaluated using the disease activity index, and colon ulceration and intestinal mucosal damage were determined by histopathological observation through HE, AB-PAS, and Masson pathological staining. The concentrations of TNF- Results: The network pharmacology results showed 108 active compounds, and 139 FMP-related targets were identified. Twenty-nine targets were identified for FMPs against UC, which included MMP9, MMP3, ESR1, PTGS1, PPARA, MPO, and NOS2. A total of 1,536 GO terms and 41 pathways were associated with FMP treatment of UC. The pharmacological evaluation showed that FMPs attenuated inflammation in AA-induced colitis by reducing the serum concentrations of TNF- Conclusion: These results suggest that FMPs control UC inflammation by regulating inflammatory cytokine concentrations. FMPs alleviate AA-induced UC by regulating microvascular permeability through the VEGF-PI3K/Akt-eNOS signaling pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.