Evidence map›Paper›PMID 24125472›Full record

ArticleBritish journal of pharmacology2014

Andrographolide suppresses RANKL-induced osteoclastogenesis in vitro and prevents inflammatory bone loss in vivo.

Z J Zhai, H W Li, G W Liu, X H Qu, B Tian, W Yan, Z Lin, T T Tang, A Qin, K R Dai

Open access · greenAbstract read
In one paragraph

Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 3 pooled it
4.8field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 3 syntheses or guidelines pooled it, 117 citations in OpenAlex.

  1. Pooled it
  2. Lipopolysaccharide-Induced Bone Loss in Rodent Models: A Systematic Review and Meta-Analysis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023
    Pooled it
  3. Molecular insights into phytochemicals exhibiting anti-arthritic activity: systematic review : John Di Battista.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Pooled it
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  20. Irisin deficiency disturbs bone metabolism.Journal of cellular physiology · 2021
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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

10 authors at 5 institutions in 2 countries.

Z J ZhaiShanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedics, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
H W Li
G W Liu
X H Qu
B Tian
W Yan
Z Lin
T T Tang
A Qin
K R Dai
Shanghai Jiao Tong University · CNAffiliated Hospital of Xuzhou Medical College · CNShanghai Ninth People's Hospital · CNUniversity of Western Australia · AUWenzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeOsteoclasts play a pivotal role in diseases such as osteoporosis, rheumatoid arthritis and tumour bone metastasis. Thus, searching for natural compounds that may suppress osteoclast formation and/or function is promising for the treatment of osteoclast-related diseases. Here, we examined changes in osteoclastogenesis and LPS-induced osteolysis in response to andrographolide (AP), a diterpenoid lactone isolated from the traditional Chinese and Indian medicinal plant Andrographis paniculata. EXPERIMENTAL APPROACH: Effects of AP on osteoclast differentiation and bone resorption were measured in vitro. Western blots and RT-PCR techniques were used to examine the underlying molecular mechanisms. The bone protective activity of AP in vivo was assessed in a mouse model of osteolysis. KEY

resultsAP concentration-dependently suppressed RANKL-mediated osteoclast differentiation and bone resorption in vitro and reduced the expression of osteoclast-specific markers, including tartrate-resistant acid phosphatase, calcitonin receptors and cathepsin K. Further molecular analysis revealed that AP impaired RANKL-induced NF-κB signalling by inhibiting the phosphorylation of TGF-β-activated kinase 1, suppressing the phosphorylation and degradation of IκBα, and subsequently preventing the nuclear translocation of the NF-κB p65 subunit. AP also inhibited the ERK/MAPK signalling pathway without affecting p38 or JNK signalling. CONCLUSIONS AND IMPLICATIONS: AP suppressed RANKL-induced osteoclastogenesis through attenuating NF-κB and ERK/MAPK signalling pathways in vitro, thus preventing bone loss in vivo. These data indicated that AP is a promising natural compound for the treatment of osteoclast-related bone diseases.

Indexed as

Disease Models, AnimalAnimalsAnti-Inflammatory Agents, Non-SteroidalBiomarkersBone and BonesBone DensityBone Density Conservation AgentsBone Marrow CellsCells, CulturedDiterpenesDown-RegulationFemaleMacrophagesMAP Kinase Signaling SystemMiceMice, Inbred C57BLandrographolideAnti-Inflammatory Agents, Non-SteroidalBiomarkersBone Density Conservation AgentsDiterpenesNF-kappa BRANK LigandRecombinant ProteinsTnfsf11 protein, mouseandrographolideERKNF-κBosteoclastosteolysis

Identifiers

PMID24125472
PMCPMC3969079
OpenAlexW1551051666

What OpenQuestion holds

Textmetadata
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.