ArticleIranian journal of pharmaceutical research : IJPR
Quercetin Induces Macrophage Polarization through PI3K-AKT Pathway in Atherosclerosis: Network Pharmacology, Molecule Docking and in vitro Analysis.
Article in Iranian journal of pharmaceutical research : IJPR. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Quercetin (QU) is a major flavonoid in multiple herbs with wide biological effects, while its role in preventing atherosclerosis progression remains largely unknown. Objectives: In this study, we aimed to uncover the effect and underlying mechanism of QU in treating atherosclerosis. Methods: Network pharmacology and protein-protein interaction analysis were conducted to predict potential targets of QU in treating atherosclerosis. Gene ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed. Cell viability, apoptosis, and cell cycle assays were conducted to evaluate the biological effects of QU on atherosclerosis-associated macrophages. Genome expression sequencing (RNA-seq) was performed to identify differentially expressed genes and regulated pathways after QU treatments. Macrophage differentiation and fluorescence-activated cell sorting (FACS), western blot, and reverse transcription quantitative polymerase chain reaction (RT-qPCR) were further performed to verify the results of RNA-seq and the effects of QU on regulating the indicated pathway. Results: In this study, 180 potential targets were identified by network pharmacology analysis, and multiple anti-inflammatory pathways were enriched in QU treating atherosclerosis. Our data also indicated that QU promotes macrophage cell viability by reducing cell apoptosis and cell cycle arrest in an atherosclerosis-associated macrophage cell model. Additionally, RNA-seq revealed that the PI3K-AKT pathway might be the significantly upregulated pathway after QU treatment in macrophages to induce M2 polarization, which was further verified by protein and RNA detection. Conclusions: Taken together, we are the first to combine multiple database analyses and genome expression data to uncover the protective effect of QU in treating atherosclerosis by inducing M2 polarization through regulating the PI3K-AKT pathway.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.