Evidence map›Paper›PMID 37999887›Full record

ArticleChinese journal of integrative medicine2024

Paeoniflorin, the Main Monomer Component of Paeonia lactiflora, Exhibits Anti-inflammatory Properties in Osteoarthritis Synovial Inflammation.

Pu Chen, Jun Zhou, An-Min Ruan, Yu-Feng Ma, Qing-Fu Wang

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Article in Chinese journal of integrative medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.7field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 15 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Pu ChenDepartment of Orthopaedic Surgery, Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing, 100029, China.
Jun ZhouDepartment of Orthopaedic Surgery, Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing, 100029, China.
An-Min RuanDepartment of Orthopaedic Surgery, Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing, 100029, China.
Yu-Feng MaDepartment of Orthopaedic Surgery, Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing, 100029, China.
Qing-Fu WangDepartment of Orthopaedic Surgery, Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing, 100029, China. 13910052566@163.com.
Beijing University of Chinese Medicine · CNAerospace Center Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo explore the mechanism of paeoniflorin (PF) on osteoarthritis (OA) synovial inflammation from network pharmacology to experimental pharmacology.

methodsTargets of OA were constructed by detecting the database of network database platforms (Therapeutic Target database, DrugBank and GeneCards), and the targets of PF were constructed by PubChem and Herbal Ingredients' Targets database. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of these co-targeted genes were conducted via Database for Annotation, Visualization, and Integrated Discovery (DAVID) database, and protein-protein interaction (PPI) networks were conducted via the search tool for the retrieval of interacting genes (STRING) database. Cell counting kit-8 (CCK-8) assay was performed to assess the potential toxicity of PF on human OA fibroblast-like synoviocytes (FLS), quantitative real-time polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA) and Western blot were used to verify the potential mechanism of PF in synovial inflammation.

resultsTwenty-six co-targeted genes were identified. GO enrichment results showed that these co-targeted genes were most likely localized in the cytoplasm, and the biological processes mainly involved 'cellular response to hypoxia' 'lipopolysaccharide (LPS)-mediated signaling pathway' and 'positive regulation of gene expression'. KEGG pathway analysis indicated that these co-targeted genes may function through pathways associated with 'hypoxia-inducible factor-1 (HIF-1) signaling pathway' and 'tumor-necrosis factor (TNF) signaling pathway'. The PPI network showed that the top 3 hub genes were TP53, TNF, and CASP3. Molecular docking results showed that PF was well docking with TNF. CCK-8 showed no potential toxicity of 10, 20 and 50 µmol/L PF on human OA FLS. And PF significantly decreased the expression levels of interleukin-1 β, interleukin-6, TNF-α matrix metalloproteinase 13 (MMP13), and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) and TNF-α in LPS-induced OA FLS.

conclusionPF exhibited potent anti-inflammatory effect in OA synovial inflammation.

Indexed as

Anti-Inflammatory AgentsGlucosidesMonoterpenesOsteoarthritisPaeoniaProtein Interaction MapsGene OntologyGlycosidesHumansInflammationSynovial MembraneSynoviocytesAnti-Inflammatory AgentsGlucosidesGlycosidesMonoterpenespeoniflorinnetwork pharmacologyosteoarthritisPaeonia lactiflorapaeoniflorinsynovial inflammationtumor necrosis factor-α

Identifiers

PMID37999887
OpenAlexW4388969978

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Registered trials

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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.