Evidence map›Paper›PMID 36253872›Full record

ArticleEuropean journal of medical research2022

Icariin alleviates osteoarthritis through PI3K/Akt/mTOR/ULK1 signaling pathway.

Yan Chen, Xiaoli Pan, Jing Zhao, Chunyan Li, Yupei Lin, Yu Wang, Xu Liu, Mei Tian

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of medical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
5.3field-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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.

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  12. The Mechanism of Icariin in Regulating BMSCs for Treating Osteoporosis: A Review.Endocrine, metabolic & immune disorders drug targets · 2026
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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

8 authors at 2 institutions in 1 country.

Yan ChenDepartment of Rheumatology and Immunology Department, Zunyi Medical University, Zunyi, 563006, China.
Xiaoli PanDepartment of Rheumatology and Immunology Department, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Huichuan District, Zunyi, 563003, China.
Jing ZhaoDepartment of Rheumatology and Immunology Department, Zunyi Medical University, Zunyi, 563006, China.
Chunyan LiDepartment of Rheumatology and Immunology Department, Zunyi Medical University, Zunyi, 563006, China.
Yupei LinDepartment of Rheumatology and Immunology Department, Zunyi Medical University, Zunyi, 563006, China.
Yu WangDepartment of Rheumatology and Immunology Department, Zunyi Medical University, Zunyi, 563006, China.
Xu LiuDepartment of Rheumatology and Immunology Department, Peking University People's Hospital, Beijing, 100044, China.
Mei TianDepartment of Rheumatology and Immunology Department, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Huichuan District, Zunyi, 563003, China. 348820517@qq.com.
Zunyi Medical University · CNPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThis study aims to investigate the effects of Icariin (ICA) on interleukin-1β (IL-1β)-induced osteoarthritis (OA) and its potential mechanism of action.

methodsSW1353 chondrocytes were pretreated with ICA for 2 h, followed by stimulation with IL-1β to mimic OA. Expression levels of matrix metalloproteinases (MMP-3) and collagen II were determined using real-time PCR and Western blot assays. Autophagy activation (by ICA) or inhibition (by shRNA) was determined based on the expression levels of ULK1, Beclin-1, LC3-II/I, and p62, using Western blot analysis. The phosphorylation levels of PI3K, Akt, mTOR, and ULK1 were also detected using Western blot analysis.

resultsIL-1β increased MMP-3 overproduction, induced collagen II degradation, and reduced the level of autophagy-associated proteins, including ULK1, Beclin-1, and LC3-II/I. In contrast, ICA pretreatment attenuated IL-1β-induced MMP-3 overproduction, increased collagen II expression, and induced expression of autophagy-related proteins. ICA also decreased PI3K, Akt, and mTOR phosphorylation, increased the production of ULK1, and induced autophagy. Short hairpin RNA-mediated knockdown of ULK1 led to activation of the PI3K/Akt/mTOR pathway, which reversed the protective effects of ICA.

conclusionsOur findings indicate that ICA can induce autophagy by regulating the PI3K/AKT/mTOR/ULK1 signaling pathway. This study suggests that ICA may be effective for treating OA.

Indexed as

OsteoarthritisProto-Oncogene Proteins c-aktAutophagyAutophagy-Related Protein-1 HomologBeclin-1ChondrocytesCollagenFlavonoidsHumansInterleukin-1betaIntracellular Signaling Peptides and ProteinsMatrix Metalloproteinase 3Phosphatidylinositol 3-KinasesRNA, Small InterferingSignal TransductionTOR Serine-Threonine KinasesAutophagy-Related Protein-1 HomologBeclin-1CollagenFlavonoidsicariinInterleukin-1betaIntracellular Signaling Peptides and ProteinsMatrix Metalloproteinase 3MTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Small InterferingTOR Serine-Threonine KinasesULK1 protein, humanAutophagyChondrocytesIcariinInterleukin-1βPI3K/Akt/mTOR/ULK1

Identifiers

PMID36253872
PMCPMC9575285
OpenAlexW4306404424

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.