Evidence map›Paper›PMID 39152382›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

Epimedin A inhibits the PI3K/AKT/NF-κB signalling axis and osteoclast differentiation by negatively regulating TRAF6 expression.

Jun Li, Jia J Wei, Cen H Wu, Tao Zou, Hong Zhao, Tian Q Huo, Cheng J Wei, Ting Yang

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

15 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

8 authors.

Jun LiDepartment of Spine Surgery, Changzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Changzhou, 213000, People's Republic of China. lijun331188@163.com.ORCID 0009-0004-4092-2365
Jia J WeiDepartment of Orthopedics, Yunnan Province Hospital of Traditional Chinese Medicine, Kunming, 650000, People's Republic of China.
Cen H WuDepartment of Spine Surgery, Changzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Changzhou, 213000, People's Republic of China.
Tao ZouDepartment of Spine Surgery, Changzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Changzhou, 213000, People's Republic of China.
Hong ZhaoDepartment of Spine Surgery, Changzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Changzhou, 213000, People's Republic of China.
Tian Q HuoDepartment of Spine Surgery, Changzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Changzhou, 213000, People's Republic of China.
Cheng J WeiDepartment of Orthopedics, Jiangsu Province Hospital of Traditional Chinese Medicine Affiliated to Nanjing Universityof Chinese Medicine, Nanjing, 210000, People's Republic of China. hongzhao1982@163.com.
Ting YangDepartment of Rheumatology, Changzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Changzhou, 213000, People's Republic of China.

Funding

Changzhou Municipal Health Commission No.ZD202222
6 · The paper itself

Abstract

backgroundEpimedin A (EA) has been shown to suppress extensive osteoclastogenesis and bone resorption, but the effects of EA remain incompletely understood. The aim of our study was to investigate the effects of EA on osteoclastogenesis and bone resorption to explore the corresponding signalling pathways.

methodsRats were randomly assigned to the sham operation or ovariectomy group, and alendronate was used for the positive control group. The therapeutic effect of EA on osteoporosis was systematically analysed by measuring bone mineral density and bone biomechanical properties. In vitro, RAW264.7 cells were treated with receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) to induce osteoclast differentiation. Cell viability assays, tartrate-resistant acid phosphatase (TRAP) staining, and immunofluorescence were used to elucidate the effects of EA on osteoclastogenesis. In addition, the expression of bone differentiation-related proteins or genes was evaluated using Western blot analysis or quantitative polymerase chain reaction (PCR), respectively.

resultsAfter 3 months of oral EA intervention, ovariectomized rats exhibited increased bone density, relative bone volume, trabecular thickness, and trabecular number, as well as reduced trabecular separation. EA dose-dependently normalized bone density and trabecular microarchitecture in the ovariectomized rats. Additionally, EA inhibited the expression of TRAP and NFATc1 in the ovariectomized rats. Moreover, the in vitro results indicated that EA inhibits osteoclast differentiation by suppressing the TRAF6/PI3K/AKT/NF-κB pathway. Further studies revealed that the effect on osteoclast differentiation, which was originally inhibited by EA, was reversed when the TRAF6 gene was overexpressed.

conclusionsThe findings indicated that EA can negatively regulate osteoclastogenesis by inhibiting the TRAF6/PI3K/AKT/NF-κB axis and that ameliorating ovariectomy-induced osteoporosis in rats with EA may be a promising potential therapeutic strategy for the treatment of osteoporosis.

Indexed as

Cell DifferentiationNF-kappa BOsteoclastsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTNF Receptor-Associated Factor 6AnimalsBone DensityFemaleFlavonoidsGene Expression RegulationMiceOsteogenesisOsteoporosisOvariectomyFlavonoidsNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTNF Receptor-Associated Factor 6Epimedin AOsteoclastogenesisOsteoporosisPI3K/AKT/NF-κB signalling pathwayTRAF6

Identifiers

PMID39152382
PMCPMC11330075

What Socratic holds

Textmetadata
LicenceCC BY
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Registered trials

None linked

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.