Evidence map›Paper›PMID 33442237›Full record

ArticleDrug design, development and therapy2021

Pristimerin Protects Against OVX-Mediated Bone Loss by Attenuating Osteoclast Formation and Activity via Inhibition of RANKL-Mediated Activation of NF-κB and ERK Signaling Pathways.

Xuedong Li, Xixi Lin, Zuoxing Wu, Yuangang Su, Jiamin Liang, Runfeng Chen, Xue Yang, Lei Hou, Jinmin Zhao, Qian Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

Xuedong Li *Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Xixi Lin *Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Zuoxing WuSchool of Medicine, Xiamen University, Xiamen, Fujian 361102, People's Republic of China.
Yuangang SuGuangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Jiamin LiangGuangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Runfeng ChenGuangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Xue YangGuangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Lei HouDepartment of Cardiology, Tongren Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.
Jinmin ZhaoGuangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Qian LiuResearch Centre for Regenerative Medicine, Orthopaedic Department, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Feng XuGuangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi 530021, People's Republic of China.
Guangxi Medical University · CNFirst Affiliated Hospital of GuangXi Medical University · CNTongren Hospital · CNXiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionOsteoporosis is an osteolytic bone condition characterized by decreased bone strength and increased bone fragility. It is the result of elevated formation or activity of bone-resorbing osteoclasts. Although current therapeutic agents are efficacious against osteoclast-mediated bone loss, detrimental side effects preclude the long-term use of these agents. Pristimerin (PRI) is a naturally occurring quinone-methide triterpenoid that has been revealed to exert anti-inflammatory and anti-tumor effects via regulating various signaling cascades including NF-κB and MAPK activation.

methodsThe bone marrow macrophages were used to confirm the anti-osteoclastic and anti-resorptive functions of PRI in vitro. An in vivo ovariectomy (OVX) model was applied to verify the function of PRI protecting bone loss.

resultsPRI abolished the early activation of NF-κB and ERK MAPK signal cascades thereby thwarting the downstream expression of c-Fos and NFATc1, which prevented the production of mature osteoclasts. In vivo, PRI protects mice against ovariectomy (OVX)-mediated bone loss by diminishing osteoclast formation and bone resorptive activity.

conclusionOur study shows that PRI demonstrates therapeutic potential in the effective treatment against osteoclast-induced osteolytic diseases like osteoporosis.

Indexed as

AnimalsBone ResorptionCells, CulturedCell SurvivalFemaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLNF-kappa BOsteoclastsOsteoporosisOvariectomyPentacyclic TriterpenesProtective AgentsTranscription Factor RelAcelastrol methyl esterNF-kappa BPentacyclic TriterpenesProtective AgentsRELA protein, humanTranscription Factor RelAERKNF-κBosteoclastosteoporosispristimerin

Identifiers

PMID33442237
PMCPMC7800467
OpenAlexW3119137512

What OpenQuestion holds

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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 OpenQuestion graph.