Evidence map›Paper›PMID 28350048›Full record

ArticleInternational journal of molecular medicine2017

Silybin attenuates LPS-induced lung injury in mice by inhibiting NF-κB signaling and NLRP3 activation.

Bo Zhang, Bing Wang, Shuhua Cao, Yongqiang Wang, Di Wu

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.2field-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

36 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  7. Article
  8. Silymarin and Inflammation: Food for Thoughts.Antioxidants (Basel, Switzerland) · 2024
    Review
  9. Inhibition of Phagocytosis by Silibinin in Mouse Macrophages.Current issues in molecular biology · 2023
    Article
  10. International journal of molecular sciences · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
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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

5 authors at 3 institutions in 1 country.

Bo ZhangIntensive Care Unit, Tianjin Huanhu Hospital, Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Hexi, Tianjin 300060, P.R. China.
Bing WangIntensive Care Unit, Tianjin First Center Hospital, Tianjin Ιnstitute of Εmergency Μedicine, Nankai, Tianjin 300192, P.R. China.
Shuhua CaoIntensive Care Unit, Tianjin First Center Hospital, Tianjin Ιnstitute of Εmergency Μedicine, Nankai, Tianjin 300192, P.R. China.
Yongqiang WangIntensive Care Unit, Tianjin First Center Hospital, Tianjin Ιnstitute of Εmergency Μedicine, Nankai, Tianjin 300192, P.R. China.
Di WuIntensive Care Unit, Tianjin Huanhu Hospital, Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Hexi, Tianjin 300060, P.R. China.
Tianjin Huanhu Hospital · CNTianjin Medical University · CNTianjin First Center Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Silybin is one of the main flavonoids produced by milk thistle, which has been used in the treatment of liver diseases. In this study, we examined the protective effects and possible mechanisms of action of silybin in lipopolysaccharide (LPS)‑induced lung injury and inflammation. Pre-treatment of mice with silybin significantly inhibited LPS-induced airway inflammatory cell recruitment, including macrophages, T cells and neutrophils. The production of cytokines, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in bronchoalveolar fluid and serum was also decreased following treatment with silybin. Elevated cytokine mRNA levels induced by LPS in lung tissue were all suppressed by silybin and lung histological alterations were also improved. In addition, experiments using cells indicated that silybin significantly decreased the mRNA levels and secretion of IL-1β and TNF-α in THP-1 cells. Moreover, the mechanisms responsible for these effects were attributed to the inhibitory effect of silybin on nuclear factor-κB (NF-κB) signaling and NLR family pyrin domain containing 3 (NLRP3) inflammasome activation. The data form our study thus support the utility of silybin as a potential medicine for the treatment of acute lung injury‑associated inflammation and pathological changes. Silybin exerts protective effects against lung injury by regulating NF-κB signaling and the NLRP3 inflammasome activation.

Indexed as

Acute Lung InjuryAnimalsCell LineCytokinesDisease Models, AnimalFemaleHumansInflammasomesInflammation MediatorsLipopolysaccharidesMiceNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinPhosphorylationReactive Oxygen SpeciesSignal TransductionCytokinesInflammasomesInflammation MediatorsLipopolysaccharidesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesSilybinSilymarin

Identifiers

PMID28350048
PMCPMC5403282
OpenAlexW2601031157

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.