ArticleJournal of inflammation research2025
Bioinformatics and Network Pharmacology Identify the Therapeutic Role of Guominkang in Allergic Asthma by Inhibiting PI3K/Akt Signaling.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Helper T cells and chemokines in elderly asthma - Mechanisms of airway inflammation and remodeling: A review.Biomolecules & biomedicine · 2026Review
- Comparison of Tylophora indica with Tylophora pauciflora coupled with network pharmacology of phenanthroindolizidine alkaloids sheds light on its antiallergic potential.Molecular biology reports · 2026Article
- Combining AlphaFold-based AI docking with omics technologies preliminarily unveils the mechanism of Guominkang in treating allergic rhinitis.Scientific reports · 2025Article
- Characterization and Anti-Allergic Mechanisms of Bioactive Compounds in a Traditional Chinese Medicine Prescription Using UHPLC-Q-TOF-MS/MS, Network Pharmacology and Computational Simulations.Pharmaceuticals (Basel, Switzerland) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: As a classical regulating formula, Guominkang (GMK) has been extensively employed in clinical practice to treat the allergic asthma (AA) and alleviate allergy symptoms, however, the underlying mechanism remains elusive. The aim of this study was to explored the mechanism of action through which GMK combats AA. Methods: Potential target genes for the compounds were identified from the database and subjected to functional enrichment analysis. Subsequently, a protein-protein interaction (PPI) network was constructed in order to screen the core target and confirmed by molecular docking. An asthma model was further developed in mice and airway hyperresponsiveness and lung pathological changes were observed following drug administration. The expression of PI3K and AKT proteins in lung tissues was then detected by Western blotting. Subsequently, the GSE104468 data were normalised and visualised using the R language, compared to the PI3K-Akt pathway gene set to identify overlapping genes, constructed a PPI network and analysed correlations between genes. Results: 267 compounds and 475 disease-relevant GMK targets have been obtained, primarily in the areas of chemokine binding, drug binding, and PI3K-Akt pathway modulation. Molecular docking simulations revealed that predicted targets (PI3K, TNF, IL6, AKT1, SRC, TP53, and STAT3) could be closely bonded with component of GMK. According to in vivo experiments, GMK could reduce mucus obstruction and airway inflammation ( Conclusion: Based on our findings, GMK potentially acts via the PI3K/Akt pathway and alleviates allergic symptoms in AA.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.