ArticleEvidence-based complementary and alternative medicine : eCAM2022
Network Pharmacology and Experimental Verification Revealed the Mechanism of Yiqi Jianpi Recipe on Chronic Obstructive Pulmonary Disease.
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 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
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Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: The study aimed to explore the active ingredients, targets, and mechanism of action of Yiqi Jianpi recipe (YQJPR) in the treatment of COPD based on the network pharmacology and COPD rat models. Methods: The active ingredients and targets of YQJPR were collected by TCMSP. Disease-related protein targets were obtained from GeneCards. The Venn diagram was used to show the key therapeutic targets of COPD in YQJPR. The PPI network was established by STRING, and cytoHubba plug-in was used to screen the core targets within the network. GO functional enrichment and KEGG pathway enrichment analysis were performed to describe the functions and pathways of the core targets. Cytoscape software was used to construct the ingredient-target network and the core target-enrichment pathway network. The chemical constituents of YQJPR were analyzed by HPLC-MS/MS. Results: The network pharmacology showed 152 active ingredients and 225 targets in YQJPR for the treatment of COPD. The key active ingredients were quercetin, luteolin, kaempferol, tanshinone IIA, and baicalein. The contents of quercetin and luteolin in YQJPR were quantitatively measured by HPLC-MS/MS. 22 core genes were screened, including AKT1, IL-6, JUN, VEGFA, and CASP3, which were mainly involved in BPs such as cell proliferation and differentiation, oxidative/chemical stress, and regulation of DNA-binding transcription factor activity and regulated viral infection, tumor, HIF-1, MAPK, TNF, and IL-17 pathways. Animal experiments showed that YQJPR could significantly reduce the expression of p-ERK1/2, p-Akt, c-Myc, cleaved caspase-3, and p-Stat3 in lung tissue ( Conclusion: The effects of YQJPR on COPD may involve multiple components, pathways, and targets. This study provides new ideas for further and more comprehensive exploration of the therapeutic effect of YQJPR on COPD in the future.
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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.