Evidence map›Paper›PMID 35653787›Full record

ArticleBioengineered2022

Plumbagin relieves rheumatoid arthritis through nuclear factor kappa-B (NF-κB) pathway.

Chang Shu, Jun Chen, Meiyan Lv, Yiyuan Xi, Jujia Zheng, Xiangwei Xu

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
4.6field-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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
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  13. Exploring Synergistic Inhibition of Inflammatory and Antioxidant Potential: IntegratedAdvances in pharmacological and pharmaceutical sciences · 2024
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Chang ShuDepartment of Orthopaedic, The First People's Hospital of Yongkang, Yongkang, Zhejiang, China.
Jun ChenDepartment of Pharmacy, The First People's Hospital of Yongkang, Yongkang, Zhejiang, China.
Meiyan LvDepartment of Clinical Laboratory, The First People's Hospital of Yongkang, Yongkang, Zhejiang, China.
Yiyuan XiSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Jujia ZhengSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Xiangwei XuDepartment of Pharmacy, The First People's Hospital of Yongkang, Yongkang, Zhejiang, China.ORCID 0000-0003-1775-6755
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to explore the effects of plumbagin on rheumatoid arthritis (RA) and its mechanism. The RA cell model was simulated following the treatment of interleukin-1β (IL-1β). After the treatment of various concentrations of plumbagin, the impact of plumbagin on the cell viability was examined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The collagen-induced arthritis (CIA) model was established using the solution of bovine type II collagen. Hematoxylin-eosin staining was used to observe the changes of ankle joint tissue, while enzyme-linked immunosorbent assay and western blot were applied to detect the level of inflammatory cytokines. Plumbagin inhibited the viability of human fibroblast-like synoviocytes (HFLS) at the concentration of 1 ~ 3.5 μM. The inhibitory effect of 1 μM plumbagin on cell proliferation was similar to that of methotrexate, the drug used as the positive control. Plumbagin downregulated the levels of inflammatory cytokines and matrix metalloproteinases (MMPs) in IL-1β-treated HFLS, and suppressed the activation of IκB and nuclear factor kappa-B (NF-κB) as well as the entry of p65 into the nucleus. It was also demonstrated in animal experiments that plumbagin inhibited the activation of NF-κB pathway, down-regulated the levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and MMPs, and alleviated joint damage in CIA-modeled mice. Collectively speaking, plumbagin might down-regulate the levels of inflammatory cytokines and MMPs through inhibiting the activation of the NF-κB pathway, thereby attenuating RA-induced damage to cells and joints.

Indexed as

Arthritis, ExperimentalArthritis, RheumatoidAnimalsCattleCells, CulturedCytokinesInterleukin-1betaInterleukin-6Matrix MetalloproteinasesMiceNaphthoquinonesNF-kappa BSynovial MembraneTumor Necrosis Factor-alphaCytokinesInterleukin-1betaInterleukin-6Matrix MetalloproteinasesNaphthoquinonesNF-kappa BplumbaginTumor Necrosis Factor-alphainflammationNF-κBplumbaginRheumatoid arthritis

Identifiers

PMID35653787
PMCPMC9276045
OpenAlexW4281647421

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.