Evidence map›Paper›PMID 34072123›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Cardamonin Attenuates Inflammation and Oxidative Stress in Interleukin-1β-Stimulated Osteoarthritis Chondrocyte through the Nrf2 Pathway.

Yi-Jen Peng, Jeng-Wei Lu, Chian-Her Lee, Herng-Sheng Lee, You-Hsiang Chu, Yi-Jung Ho, Feng-Cheng Liu, Chun-Jung Huang, Chia-Chun Wu, Chih-Chien Wang

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 42 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

10 authors at 5 institutions in 2 countries.

Yi-Jen PengDepartment of Pathology, National Defense Medical Center, Tri-Service General Hospital, Taipei 114, Taiwan.ORCID 0000-0003-4630-2103
Jeng-Wei LuDepartment of Biological Sciences, National University of Singapore, Singapore 117543, Singapore.ORCID 0000-0003-2128-2046
Chian-Her LeeDepartment of Orthopedics, School of Medicine, College of Medicine, Taipei Medical University Hospital, Taipei Medical University, Taipei 110, Taiwan.
Herng-Sheng LeeLaboratory Medicine, Department of Pathology, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan.
You-Hsiang ChuNational Defense Medical Center, Graduate Institute of Life Sciences, Taipei 114, Taiwan.
Yi-Jung HoNational Defense Medical Center, Graduate Institute of Life Sciences, Taipei 114, Taiwan.
Feng-Cheng LiuDepartment of Medicine, Rheumatology/Immunology and Allergy, National Defense Medical Center, Tri-Service General Hospital, Taipei 114, Taiwan.
Chun-Jung HuangDepartment of Pathology, National Defense Medical Center, Tri-Service General Hospital, Taipei 114, Taiwan.
Chia-Chun WuDepartment of Orthopedics, National Defense Medical Center, Tri-Service General Hospital, Taipei 114, Taiwan.
Chih-Chien WangDepartment of Orthopedics, National Defense Medical Center, Tri-Service General Hospital, Taipei 114, Taiwan.ORCID 0000-0003-3709-3848
Tri-Service General Hospital · TWNational Defense Medical Center · TWKaohsiung Veterans General Hospital · TWNational University of Singapore · SGTaipei Medical University Hospital · TW

Funding

Ministry of National Defense-Medical Affairs Bureau MAB-106-006Ministry of Science and Technology MOST 107-2314-B-038-088Ministry of Science and Technology MOST108-2314-B-038-082National Defense Medical Center ATSGH-C107-211National Defense Medical Center TSGH-108-089National Defense Medical Center TSGH-C107-081National Defense Medical Center TSGH-C108-113National Defense Medical Center TSGH-D-10902National Defense Medical Center TSGH-E-110232
6 · The paper itself

Abstract

Osteoarthritis (OA) is a chronic degenerative joint disease characterized by the deterioration of articular cartilage. The progression of OA leads to an increase in inflammatory mediators in the joints, thereby promoting the destruction of the cartilage matrix. Recent studies have reported on the anti-inflammatory and antioxidant properties of cardamonin, which also appears to interact with cellular targets, such as nuclear erythroid 2-related factor 2 (Nrf2), extracellular signal-regulated kinase (ERK), and mammalian target of rapamycin (mTOR) during the progression of tumors. To date, few studies have investigated the effects of cardamonin on chondrocyte inflammation. In the current study, we determined that treating interleukin-1 beta (IL-1β-stimulated chondrocyte cells) with cardamonin significantly reduced the release of nitric oxide (NO) and prostaglandin E2 (PGE2) and significantly inhibited the expression of pro-inflammatory proteins, including inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2). Cardamonin was also shown to: (1) inhibit the activation and production of matrix metalloproteinases (MMPs), (2) suppress the nuclear factor-κB (NF-κB) signaling pathway, (3) suppress the expression of toll-like receptor proteins, (4) activate the Nrf2 signaling pathway, and (5) increase the levels of antioxidant proteins heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1). The increase in antioxidant proteins led to corresponding antioxidant effects (which were abolished by Nrf2 siRNA). Our findings identify cardamonin as a candidate Nrf2 activator for the treatment and prevention of OA related to inflammation and oxidative stress.

Indexed as

cardamoninchondrocyteinterleukin-1 betaosteoarthritisoxidative stress

Identifiers

PMID34072123
PMCPMC8227809
OpenAlexW3165239352

What Socratic 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 Socratic graph.