Evidence map›Paper›PMID 32021104›Full record

ArticleDrug design, development and therapy2020

Baicalin Ameliorates Dexamethasone-Induced Osteoporosis by Regulation of the RANK/RANKL/OPG Signaling Pathway.

Ye Zhao, Hui-Ling Wang, Tong-Tong Li, Fei Yang, Chi-Meng Tzeng

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

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  16. 7-Hydroxyflavone Mitigates OsteoporosisCurrent topics in medicinal chemistry · 2025
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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 2 institutions in 1 country.

Ye ZhaoSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing 211800, People's Republic of China.
Hui-Ling WangSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing 211800, People's Republic of China.
Tong-Tong LiSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing 211800, People's Republic of China.
Fei YangSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing 211800, People's Republic of China.
Chi-Meng TzengSchool of Pharmaceutical Sciences, Nanjing Tech University, Nanjing 211800, People's Republic of China.
Nanjing Tech University · CNThe Synergetic Innovation Center for Advanced Materials · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteoporosis is a chronic bone metabolism disorder affecting millions of the world population. The RANKL/RANK/OPG signaling pathway has been confirmed to be the main regulator of osteoporosis. It is of great interest to identify appropriate therapeutic agents that can regulate the RANKL/RANK/OPG pathway. Baicalin (BA) is a well-known traditional Chinese medicine formula against various inflammatory diseases with a proven role of the RANKL/RANK/OPG pathway regulation. However, the potential effect of BA on osteoporosis and the mechanisms underlying this remain unclear. In the present study, we aimed to evaluate the efficacy of BA in the prevention of dexamethasone (DEX)-induced osteoporosis in zebrafish.

methodsIn this study, growth and development changes of zebrafish and calcein staining were assessed with a micrograph. The expression levels of RANKL and OPG and transcription factors in response to DEX induction and BA administration were evaluated by Western blotting and qRT-PCR. In addition, the intermolecular interactions of BA and RANKL were investigated by molecular docking.

resultsResults show that BA enhances the growth and development of dexamethasone (DEX)-induced osteoporosis in zebrafish larvae. Calcein staining and calcium and phosphorus determination revealed that BA ameliorates mineralization of DEX-induced osteoporosis zebrafish larvae. BA also regulates the expression of RANKL and OPG and hampers the changes in gene expression related to bone formation and resorption under the induction of DEX in zebrafish. It can be inferred by molecular docking that BA may interact directly with the extracellular domain of RANKL.

conclusionThe findings, herein, reveal that BA ameliorates DEX-induced osteoporosis by regulation of the RANK/RANKL/OPG signaling pathway.

Indexed as

AnimalsCell DifferentiationDexamethasoneDose-Response Relationship, DrugFlavonoidsLarvaMolecular Docking SimulationOsteoclastsOsteoporosisOsteoprotegerinRANK LigandReceptor Activator of Nuclear Factor-kappa BRNA, MessengerSignal TransductionZebrafishbaicalinDexamethasoneFlavonoidsOsteoprotegerinRANK LigandReceptor Activator of Nuclear Factor-kappa BRNA, MessengerBaicalinOPGosteoporosisRANKRANKL

Identifiers

PMID32021104
PMCPMC6970258
OpenAlexW2999569987

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.