Evidence map›Paper›PMID 26013831›Full record

ArticleThe Journal of biological chemistry2015

Sulforaphane Attenuates Muscle Inflammation in Dystrophin-deficient mdx Mice via NF-E2-related Factor 2 (Nrf2)-mediated Inhibition of NF-κB Signaling Pathway.

Cheng-Cao Sun, Shu-Jun Li, Cui-Li Yang, Rui-Lin Xue, Yong-Yong Xi, Liang Wang, Qian-Long Zhao, De-Jia Li

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The Journal of biological chemistry, 2015. 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 It has been retracted, and should not be counted.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 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
11.1field-weighted citation impact, top 1% 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

77 citing papers in PubMed, 149 citations in OpenAlex.

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  20. Anti-Inflammatory Activity of Three Triterpene fromInternational journal of molecular sciences · 2021
    Article

17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Cheng-Cao SunDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, 430071 Wuhan, China.
Shu-Jun LiDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, 430071 Wuhan, China.
Cui-Li YangDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, 430071 Wuhan, China.
Rui-Lin XueDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, 430071 Wuhan, China.
Yong-Yong XiDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, 430071 Wuhan, China.
Liang WangDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, 430071 Wuhan, China.
Qian-Long ZhaoDepartment of Occupational and Environmental Health, School of Public Health, Lanzhou University, 730000 Lanzhou, China.
De-Jia LiDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, 430071 Wuhan, China. Electronic address: lodjlwhu@sina.com.
Wuhan University · CNLanzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is widely distributed in patients with Duchenne muscular dystrophy and ultimately leads to progressive deterioration of muscle function with chronic muscle damage, oxidative stress, and reduced oxidative capacity. NF-E2-related factor 2 (Nrf2) plays a critical role in defending against inflammation in different tissues via activation of phase II enzyme heme oxygenase-1 and inhibition of the NF-κB signaling pathway. However, the role of Nrf2 in the inflammation of dystrophic muscle remains unknown. To determine whether Nrf2 may counteract inflammation in dystrophic muscle, we treated 4-week-old male mdx mice with the Nrf2 activator sulforaphane (SFN) by gavage (2 mg/kg of body weight/day) for 4 weeks. The experimental results demonstrated that SFN treatment increased the expression of muscle phase II enzyme heme oxygenase-1 in an Nrf2-dependent manner. Inflammation in mice was reduced by SFN treatment as indicated by decreased infiltration of immune cells and expression of the inflammatory cytokine CD45 and proinflammatory cytokines tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the skeletal muscles of mdx mice. In addition, SFN treatment also decreased the expression of NF-κB(p65) and phosphorylated IκB kinase-α as well as increased inhibitor of κB-α expression in mdx mice in an Nrf2-dependent manner. Collectively, these results show that SFN-induced Nrf2 can alleviate muscle inflammation in mdx mice by inhibiting the NF-κB signaling pathway.

Indexed as

AnimalsAnti-Inflammatory AgentsAntioxidantsDystrophinGene DeletionHeme Oxygenase-1InflammationIsothiocyanatesMaleMembrane ProteinsMiceMice, Inbred C57BLMice, Inbred mdxMuscle, SkeletalMuscular Dystrophy, DuchenneNF-E2-Related Factor 2Anti-Inflammatory AgentsAntioxidantsDystrophinHeme Oxygenase-1Hmox1 protein, mouseIsothiocyanatesMembrane ProteinsNF-E2-Related Factor 2NF-kappa BsulforaphaneSulfoxidesantioxidantinflammationNF-κBnuclear translocationoxidative stresstranscription factortransgenic mice

Identifiers

PMID26013831
PMCPMC4505027
OpenAlexW1562263022

What OpenQuestion holds

Textmetadata
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.