Evidence map›Paper›PMID 33155655›Full record

ArticleBioscience reports2020

Icariin inhibits the inflammation through down-regulating NF-κB/HIF-2α signal pathways in chondrocytes.

Pengzhen Wang, Qingqi Meng, Wen Wang, Shaoheng Zhang, Xifeng Xiong, Shengnan Qin, Jinli Zhang, Aiguo Li, Zhihe Liu

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Review
  9. Hypoxia signaling in the adipose tissue.Journal of molecular cell biology · 2025
    Review
  10. Review
  11. Review
  12. Icariin as a Treatment Proposal in Mammalian Reproduction.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  13. Review
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  15. Therapeutic Efficacy of Medicinal Plants with Allopathic Medicine in Musculoskeletal Diseases.International journal of plant, animal and environmental sciences · 2024
    Article
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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

9 authors at 1 institution in 1 country.

Pengzhen Wang *Guangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong 510220, China.
Qingqi Meng *Guangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong 510220, China.
Wen WangDepartment of Orthopaedics, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong 510220, China.
Shaoheng ZhangDepartment of Cardiology, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong 510220, China.
Xifeng XiongGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong 510220, China.
Shengnan QinGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong 510220, China.
Jinli ZhangGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong 510220, China.
Aiguo LiDepartment of Orthopaedics, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong 510220, China.
Zhihe LiuGuangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong 510220, China.
Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Articular cartilage injury or defect is a common disease and is mainly characterized by cartilage degradation because of chondrocyte inflammation. By now, there are no effective drugs and methods to protect articular cartilage from degradation. Icariin (ICA) is a typical flavonoid compound extracted from Epimedii Folium with anti-inflammatory and bone-protective effects. Our previous studies demonstrate that ICA up-regulates HIF-1α expression and glycolysis in chondrocytes and maintains chondrocyte phenotype. As another member of HIFs family, HIF-2α always plays a key role in inflammation. The effect of ICA on HIF-2α is unclear by now. In the present study, we confirmed the findings in our previous study that ICA promoted not only chondrocyte vitality and extracellular matrix (ECM) synthesis, but also the anti-inflammatory effect of ICA. In bone defect mice, ICA inhibited the expressions of NF-κB and HIF-2α. In TNF-α-treated ADTC5 chondrocytes, ICA neutralized the activation of IKK (IKK phosphorylation), the phosphorylation of IkB and NF-κB and the expression of HIF-2α. Furthermore, ICA inhibited the nucleus transfer of NF-κB and the expressions of MMP9 and ADAMTS5, two key targets of NF-κB/HIF-2α signal pathway. Taken together, the present study demonstrated that ICA may increase the vitality of chondrocytes by suppressing the inflammatory injury through the inhibition on NF-κB/HIF-2α signaling pathway. ICA is one effective candidate drug for the treatment of articular cartilage injury.

Indexed as

ADAMTS5 ProteinAnimalsAnti-Inflammatory AgentsBasic Helix-Loop-Helix ProteinsCartilage, ArticularCells, CulturedChondrocytesDisease Models, AnimalEndothelial PAS Domain-Containing Protein 1Extracellular MatrixFlavonoidsMaleMatrix Metalloproteinase 9Mice, Inbred C57BLNF-kappa BOsteoarthritisADAMTS5 ProteinAdamts5 protein, mouseAnti-Inflammatory AgentsBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1FlavonoidsicariinMatrix Metalloproteinase 9Mmp9 protein, mouseNF-kappa BchondrocyteIcariin (ICA)inflammationNF-κB/HIF-2α

Identifiers

PMID33155655
PMCPMC7685011
OpenAlexW3097732806

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.