Evidence map›Paper›PMID 24324641›Full record

ArticlePloS one2013

Acteoside suppresses RANKL-mediated osteoclastogenesis by inhibiting c-Fos induction and NF-κB pathway and attenuating ROS production.

Seung-Youp Lee, Keun-Soo Lee, Sea Hyun Yi, Sung-Ho Kook, Jeong-Chae Lee

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

38 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
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  6. A review ofFrontiers in pharmacology · 2024
    Review
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  12. The pharmacokinetic property and pharmacological activity of acteoside: A review.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022
    Review
  13. Review
  14. The Brown AlgaeNutrients · 2022
    Article
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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 1 institution in 1 country.

Seung-Youp LeeResearch Institute of Clinical Medicine of Chonbuk National University, Biomedical Research Institute of Chonbuk National University Hospital, Jeonju, Chonbuk, South Korea ; Department of Orthodontics, Institute of Oral Biosciences and School of Dentistry, Chonbuk National University, Jeonju, Chonbuk, South Korea.
Keun-Soo Lee
Sea Hyun Yi
Sung-Ho Kook
Jeong-Chae Lee
Jeonbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous studies have reported that inflammatory cytokines are important mediators for osteoclastogenesis, thereby causing excessive bone resorption and osteoporosis. Acteoside, the main active compound of Rehmannia glutinosa, which is used widely in traditional Oriental medicine, has anti-inflammatory and antioxidant potentials. In this study, we found that acteoside markedly inhibited osteoclast differentiation and formation from bone marrow macrophages (BMMs) and RAW264.7 macrophages stimulated by the receptor activator of nuclear factor-kappaB (NF-κB) ligand (RANKL). Acteoside pretreatment also prevented bone resorption by mature osteoclasts in a dose-dependent manner. Acteoside (10 µM) attenuated RANKL-stimulated activation of p38 kinase, extracellular signal-regulated kinases, and c-Jun N-terminal kinase, and also suppressed NF-κB activation by inhibiting phosphorylation of the p65 subunit and the inhibitor κBα. In addition, RANKL-mediated increases in the expression of c-Fos and nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1) and in the production of tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 were apparently inhibited by acteoside pretreatment. Further, oral acteoside reduced ovariectomy-induced bone loss and inflammatory cytokine production to control levels. Our data suggest that acteoside inhibits osteoclast differentiation and maturation from osteoclastic precursors by suppressing RANKL-induced activation of mitogen-activated protein kinases and transcription factors such as NF-κB, c-Fos, and NFATc1. Collectively, these results suggest that acteoside may act as an anti-resorptive agent to reduce bone loss by blocking osteoclast activation.

Indexed as

AnimalsAntioxidantsBone Marrow CellsBone ResorptionCell DifferentiationCell SurvivalFemaleGene Expression RegulationGlucosidesInterleukin-1betaInterleukin-6Interleukin-6 InhibitorsMacrophagesMiceMice, Inbred ICRNFATC Transcription FactorsacteosideAntioxidantsGlucosidesInterleukin-1betaInterleukin-6Interleukin-6 InhibitorsNfatc1 protein, mouseNFATC Transcription FactorsNF-kappa Bp38 Mitogen-Activated Protein KinasesPhenolsPolyphenolsProto-Oncogene Proteins c-fosRANK LigandReactive Oxygen SpeciesTnfsf11 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID24324641
PMCPMC3851776
OpenAlexW2150240428

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.