Evidence map›Paper›PMID 35228997›Full record

ArticleJournal of orthopaedic translation2022

Puerarin specifically disrupts osteoclast activation via blocking integrin-β3 Pyk2/Src/Cbl signaling pathway.

Zuocheng Qiu, Ling Li, Yuying Huang, Keda Shi, Lizhong Zhang, Cuishan Huang, Jiechao Liang, Qingqiang Zeng, Jiali Wang, Xiangjiu He and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of orthopaedic translation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.

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  17. The supplementation ofFood science & nutrition · 2024
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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

12 authors at 5 institutions in 2 countries.

Zuocheng QiuTranslational Medicine R&D Center, Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518057, China.
Ling LiTranslational Medicine R&D Center, Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518057, China.
Yuying HuangSchool of Pharmacy, Guangdong Pharmaceutical University, Guangzhou, 510006, China.
Keda ShiTranslational Medicine R&D Center, Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518057, China.
Lizhong ZhangTranslational Medicine R&D Center, Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518057, China.
Cuishan HuangTranslational Medicine R&D Center, Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518057, China.
Jiechao LiangTranslational Medicine R&D Center, Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518057, China.
Qingqiang ZengTranslational Medicine R&D Center, Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518057, China.
Jiali WangSchool of Biomedical Engineering, Sun Yat-sen University, Guangzhou, 510275, China.
Xiangjiu HeSchool of Pharmacy, Guangdong Pharmaceutical University, Guangzhou, 510006, China.
Ling QinTranslational Medicine R&D Center, Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518057, China.
Xinluan WangTranslational Medicine R&D Center, Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518057, China.
Chinese Academy of Sciences · CNChinese University of Hong Kong · HKGuangdong Pharmaceutical University · CNJinan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveGiven the limitations of current anti-resorption agents for postmenopausal osteoporosis, there is a need for alternatives without impairing coupling crosstalk between bone resorption and bone formation ie. osteoclastogenesis. Puerarin, a unique C-glycoside isoflavonoid, was found to be able to prevent bone loss by inhibiting bone resorption, but the underlying mechanism was controversial. In this study, we investigated the effects of puerarin on osteoclastic differentiation, activation and bone resorption and its underlying molecular mechanism

methods

resultsPuerarin significantly inhibited osteoclast activation and bone resorption, without affecting osteoclastogenesis or apoptosis. In terms of mechanism, the expressions of protein of integrin-β3 and phosphorylations of Src, Pyk2 and Cbl were lower in puerarin group than those in the control group. Oral administration of puerarin prevented OVX-induced trabecular bone loss and significantly improved bone strength in rats. Moreover, puerarin significantly decreased trap positive osteoclast numbers and serum TRAP-5b, CTx1, without affecting bone formation rate.

conclusionsCollectively, puerarin prevented the bone loss in OVX rat through suppression of osteoclast activation and bone resorption, by inhibiting integrin-β3-Pyk2/Cbl/Src signaling pathway, without affecting osteoclasts formation or apoptosis. TRANSLATIONAL POTENTIAL OF THIS ARTICLE: These results demonstrate the unique mechanism of puerarin on bone metabolism and provide a novel agent for prevention of postmenopausal osteoporosis.

Indexed as

Amino-terminal propeptide of type I collagen, RANKLAtp6v0d2, ATPase H ​+ ​Transporting V0 Subunit D2BMD, Bone mineral densityBMMs, Bone marrow monocyte cellsBS, Bone surfaceBV/TV, Bone volume/tissue volumeCarbonic anhydrase II, Cs. Thcarboxyl-terminal telopeptides of type I collagen, CLCN7Cathepsin K, E2: 17-β estradiolc-Fos: Proto-oncogene C-Fos, Ct. ArCharge-coupled Cl-channel, CA IIConnectivity density, CTSKCortical area, CTx1Cortical thickness, Conn. DEc. Pm, Endocortical perimeterER, Estrogen receptorF-actin ringIntegrin-β3Luminescence, SDMarrow area, MRMMatrix metalloproteinase-9, N. OcM-CSF, Macrophage colony-stimulating factorMultiple reaction monitoring, MMP9Nuclear factor of activated T cells 1, TRAP-5bNumber of trap positive osteoclasts, NFATc1Osteoclast activationOsteoclasts surface, P1NPOsteoclast stimulatory transmembrane protein, OPGOsteoprotegerin, Oc. SOVX, ovariectomizedPuerarinPyk2/Cbl/Srcrat bone marrow-derived mesenchymal stem cells. Tb. N, Trabecular numberReceptor activator of nuclear factor κ-B ligand, RLUSprague–Dawley, rBMSCSrc: Proto-oncogene tyrosine-protein kinase Src, Ma. ArTartrate-resistant acid phosphatase 5b, OC-STAMPTb. Sp, Trabecular separationTb. Th, Trabecular thicknessTRAF6, TNF-receptor-associated factor 6TRAP, Tartrate resistant acid phosphataseTUNEL, Terminal deoxynucleotidyl transferase dUTP nick end labeling

Identifiers

PMID35228997
PMCPMC8858883
OpenAlexW4213161726

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.