Evidence map›Paper›PMID 24066131›Full record

ArticlePloS one2013

Sinomenine suppresses osteoclast formation and Mycobacterium tuberculosis H37Ra-induced bone loss by modulating RANKL signaling pathways.

Xiaojuan Li, Longgang He, Yiping Hu, Heng Duan, Xianglian Li, Suiyi Tan, Min Zou, Chunping Gu, Xiangzhou Zeng, Le Yu and 2 more

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 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 23% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Multimodal imaging fusion and machine learning model development: differential diagnosis of spinal inflammatory lesions using combined CT hounsfield units and MRI features.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026
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  7. Article
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  9. Review
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  14. Article
  15. Article
  16. Review
  17. Roles of Mitogen-Activated Protein Kinases in Osteoclast Biology.International journal of molecular sciences · 2018
    Review
  18. Article
  19. Article
  20. Comparative Studies of Different Extracts fromEvidence-based complementary and alternative medicine : eCAM · 2018
    Article
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

12 authors at 2 institutions in 2 countries.

Xiaojuan LiSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, China.
Longgang He
Yiping Hu
Heng Duan
Xianglian Li
Suiyi Tan
Min Zou
Chunping Gu
Xiangzhou Zeng
Le Yu
Jiake Xu
Shuwen Liu
Southern Medical University · CNUniversity of Western Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Receptor activator of NF-κB ligand (RANKL) is essential for osteoclastogenesis. Targeting RANKL signaling pathways has been an encouraging strategy for treating lytic bone diseases such as osteoporosis and rheumatoid arthritis (RA). Sinomenine (SIN), derived from Chinese medicinal plant Sinomenioumacutum, is an active compound to treat RA, but its effect on osteoclasts has been hitherto unknown. In the present study, SIN was found to ameliorate M. tuberculosis H37Ra (Mt)-induced bone loss in rats with a decreased serum level of TRACP5b and RANKL, and an increased level of osteoprotegerin (OPG). In vitro study also showed that SIN could inhibit RANKL-induced osteoclast formation and bone resorption. The osteoclastic specific marker genes induced by RANKL including c-Src, MMP-9, TRACP were inhibited by SIN in a dose dependent manner. Signal transduction studies showed that SIN could obviously reduce the expression of RANK adaptor molecule TRAF6 and down-regulate RANKL-induced NF-κB activation. It decreased the RANKL-induced p38, JNK posphorylation but not ERK1/2 posphorylation. SIN could also reduce RANKL-mediated calcium influx which is associated with TRAF6/c-Src complex. Finally, SIN suppressed RANKL induced AP-1 and NFAT transcription, as well as the gene expression of NFATc1 and AP-1 components (Fra-1, Fra-2, c-Fos). The protein expression of c-Fos and TRAF6 were also inhibited by SIN after RANKL stimulation. Taken together, SIN could attenuate osteoclast formation and Mt-induced bone loss by mediating RANKL signaling pathways.

Indexed as

AnimalsBone ResorptionFemaleMiceMice, Inbred BALB CMorphinansMycobacterium tuberculosisOsteoclastsRANK LigandRatsRats, Sprague-DawleyReceptor Activator of Nuclear Factor-kappa BSignal TransductionTNF Receptor-Associated Factor 6MorphinansRANK LigandReceptor Activator of Nuclear Factor-kappa BsinomenineTNF Receptor-Associated Factor 6

Identifiers

PMID24066131
PMCPMC3774760
OpenAlexW2112887858

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.