Evidence map›Paper›PMID 30319404›Full record

ArticleFrontiers in pharmacology2018

Chelerythrine Attenuates the Inflammation of Lipopolysaccharide-Induced Acute Lung Inflammation Through NF-κB Signaling Pathway Mediated by Nrf2.

Lu Fan, Ye Fan, Li Liu, Weiwei Tao, Xin Shan, Yu Dong, Lin Li, Sen Zhang, Hanqing Wang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Review
  6. Article
  7. Article
  8. Sanguinarine-Chelerythrine fromPharmaceutics · 2025
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  9. Recent Advances in Alkaloids fromMolecules (Basel, Switzerland) · 2024
    Review
  10. Article
  11. Alkaloids inFrontiers in pharmacology · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Inferring Therapeutic Targets inLife (Basel, Switzerland) · 2022
    Article
  16. Article
  17. Review
  18. Article
  19. Sanguinarine-Chelerythrine Fraction ofOxidative medicine and cellular longevity · 2022
    Article
  20. Article
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

9 authors at 4 institutions in 1 country.

Lu FanSchool of Medicine and Life Sciences, Nanjing University of Chinese Medicine, Nanjing, China.
Ye FanDepartment of Emergency Medicine, Nanjing General Hospital/Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
Li LiuSchool of Pharmacy, Guangdong Medical University, Dongguan, China.
Weiwei TaoCenter for Translational Systems Biology and Neuroscience, School of Basic Biomedical Science, Nanjing University of Chinese Medicine, Nanjing, China.
Xin ShanCenter for Translational Systems Biology and Neuroscience, School of Basic Biomedical Science, Nanjing University of Chinese Medicine, Nanjing, China.
Yu DongCenter for Translational Systems Biology and Neuroscience, School of Basic Biomedical Science, Nanjing University of Chinese Medicine, Nanjing, China.
Lin LiCenter for Translational Systems Biology and Neuroscience, School of Basic Biomedical Science, Nanjing University of Chinese Medicine, Nanjing, China.
Sen ZhangCenter for Translational Systems Biology and Neuroscience, School of Basic Biomedical Science, Nanjing University of Chinese Medicine, Nanjing, China.
Hanqing WangSchool of Medicine and Life Sciences, Nanjing University of Chinese Medicine, Nanjing, China.
Nanjing University of Chinese Medicine · CNGuangdong Medical College · CNNanjing University · CNNingxia Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chelerythrine (CH), is a kind of benzo[c] phenanthridine alkaloid isolated from plants such as Chelidonium, with pharmacological activities as antitumor, antibiosis and anti-inflammation. However, few studies have demonstrated whether CH could protect against lipopolysaccharide (LPS)-induced acute lung injury (ALI), and the underlying mechanism is also uncertain. The purpose of the present study was to investigate the anti-inflammatory effects of CH on LPS-induced ALI in mice and in RAW264.7 cells. In this study, we demonstrated that treatment with CH significantly ameliorated LPS-induced pathological changes in the lung. CH also attenuated LPS-induced W/D ratio, inflammatory cell infiltration. Meanwhile, LPS-induced Tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), and interleukin 1β (IL-1β) production and oxidative stress were markedly suppressed by CH. Furthermore, western blot showed that CH suppressed LPS-stimulated inflammation of RAW264.7 cells through activation of nuclear factor kappa-B (NF-κB) pathway. Knocking down of nuclear factor erythroid 2-related factor 2 (Nrf2) led to the reduction of nuclear translocation of the NF-κB p65, which triggered inflammation. These experimental results provided evidence that CH could be a potential therapeutic candidate for the intervention of ALI caused by LPS.

Indexed as

ALIchelerythrineinflammationLPSNF-κBNrf2

Identifiers

PMID30319404
PMCPMC6169195
OpenAlexW2893332751

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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.