Evidence map›Paper›PMID 37612419›Full record

ArticleScientific reports2023

Cardamonin protects against iron overload induced arthritis by attenuating ROS production and NLRP3 inflammasome activation via the SIRT1/p38MAPK signaling pathway.

Shaocong Li, Qi He, Baihao Chen, Jiaxu Zeng, Xiangyun Dou, Zhaofeng Pan, Jiacong Xiao, Miao Li, Fanchen Wang, Chuyi Chen and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
5.1field-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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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  12. Physiological and molecular profiling unveils oat (Frontiers in plant science · 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

14 authors at 2 institutions in 1 country.

Shaocong Li *First School of Clinical Medicine, Guangzhou University of Chinese Medicine, 12 Jichang Road, Baiyun Area, , Guangzhou, 510405, People's Republic of China.
Qi He *First School of Clinical Medicine, Guangzhou University of Chinese Medicine, 12 Jichang Road, Baiyun Area, , Guangzhou, 510405, People's Republic of China.
Baihao Chen *First School of Clinical Medicine, Guangzhou University of Chinese Medicine, 12 Jichang Road, Baiyun Area, , Guangzhou, 510405, People's Republic of China.
Jiaxu ZengFirst School of Clinical Medicine, Guangzhou University of Chinese Medicine, 12 Jichang Road, Baiyun Area, , Guangzhou, 510405, People's Republic of China.
Xiangyun DouFirst School of Clinical Medicine, Guangzhou University of Chinese Medicine, 12 Jichang Road, Baiyun Area, , Guangzhou, 510405, People's Republic of China.
Zhaofeng PanFirst School of Clinical Medicine, Guangzhou University of Chinese Medicine, 12 Jichang Road, Baiyun Area, , Guangzhou, 510405, People's Republic of China.
Jiacong XiaoFirst School of Clinical Medicine, Guangzhou University of Chinese Medicine, 12 Jichang Road, Baiyun Area, , Guangzhou, 510405, People's Republic of China.
Miao LiFirst School of Clinical Medicine, Guangzhou University of Chinese Medicine, 12 Jichang Road, Baiyun Area, , Guangzhou, 510405, People's Republic of China.
Fanchen WangFirst School of Clinical Medicine, Guangzhou University of Chinese Medicine, 12 Jichang Road, Baiyun Area, , Guangzhou, 510405, People's Republic of China.
Chuyi ChenFirst School of Clinical Medicine, Guangzhou University of Chinese Medicine, 12 Jichang Road, Baiyun Area, , Guangzhou, 510405, People's Republic of China.
Yuewei LinFirst School of Clinical Medicine, Guangzhou University of Chinese Medicine, 12 Jichang Road, Baiyun Area, , Guangzhou, 510405, People's Republic of China.
Xintian WangFirst School of Clinical Medicine, Guangzhou University of Chinese Medicine, 12 Jichang Road, Baiyun Area, , Guangzhou, 510405, People's Republic of China.
Haibin WangDepartment of Orthopaedics, The First Affiliated Hospital, Guangzhou University of Chinese Medicine, 16 Jichang Road, Baiyun Area, Guangzhou, 510405, People's Republic of China. hipknee@163.com.
Jianfa ChenDepartment of Orthopaedics, The First Affiliated Hospital, Guangzhou University of Chinese Medicine, 16 Jichang Road, Baiyun Area, Guangzhou, 510405, People's Republic of China. 13760793784@163.com.
Guangzhou University of Chinese Medicine · CNFirst Affiliated Hospital of Guangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron homeostasis plays an essential role in joint health, while iron overload can cause damage and death of cartilage cells. Cardamonin (CAR) is a substance found in the fruit of the chasteberry plant and has anti-inflammatory and anti-tumor activities. We first administered iron dextran (500 mg/kg) intraperitoneally to establish an iron overload mouse model and surgically induced osteoarthritis. The extent of OA and iron deposition were assessed using Micro-ct, Safranin-O/fast green staining, H&E staining, and Prussian Blue 10 weeks later. We administered primary chondrocytes with Ferric Ammonium Citrate (FAC) to evaluate the chondrocyte changes. Chondrocytes were identified in vitro by toluidine blue staining, and chondrocyte viability was evaluated by CCK-8. The rate of apoptosis was determined by Annexin V-FITC/PI assay. The mechanism of action of CAR was verified by adding the SIRT1 inhibitor EX527, and the expression of SIRT1 and MAPK signaling pathways was detected by Western blot. Iron overload also promoted chondrocyte apoptosis, a process that was reversed by CAR. In addition, CAR reduced NLRP3 inflammasome production via the SIRT1-MAPK pathway, and the SIRT1 inhibitor EX527 inhibited the treatment of OA by CAR.CAR inhibited cartilage degeneration induced by iron overload both in vivo and in vitro. Besides, our study showed that iron overload not only inhibited type II collagen expression but also induced MMP expression by catalyzing the generation of NLRP3 inflammasome. Our results suggest that CAR can treat KOA by promoting SIRT1 expression and inhibiting p38MAPK pathway expression to reduce the production of NLRP3 inflammasome vesicles.

Indexed as

InflammasomesOsteoarthritisAnimalsChalconesIronMiceNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesSignal TransductionSirtuin 1cardamoninChalconesInflammasomesIronNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesSirtuin 1

Identifiers

PMID37612419
PMCPMC10447427
OpenAlexW4386092748

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.