Evidence map›Paper›PMID 28216638›Full record

ArticleScientific reports2017

Thymoquinone: An IRAK1 inhibitor with in vivo and in vitro anti-inflammatory activities.

Muhammad Jahangir Hossen, Woo Seok Yang, Daewon Kim, Adithan Aravinthan, Jong-Hoon Kim, Jae Youl Cho

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
–field-weighted citation impact
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

76 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Foods (Basel, Switzerland) · 2026
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  7. Exploring the Multifaceted Phytochemical Profile ofPharmaceuticals (Basel, Switzerland) · 2026
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  8. Immunomodulatory Effects of Medicinal Plants.Advances in experimental medicine and biology · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Analysis of Pharmacological Properties ofLife (Basel, Switzerland) · 2025
    Review
  13. Article
  14. Antioxidant and Anti-Inflammatory Activities ofMolecules (Basel, Switzerland) · 2025
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Evolution of radiation-induced dermatitis treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Review

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

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

6 authors.

Muhammad Jahangir HossenDepartment of Genetic Engineering, Sungkyunkwan University, Suwon 16419, Republic of Korea.
Woo Seok YangDepartment of Genetic Engineering, Sungkyunkwan University, Suwon 16419, Republic of Korea.
Daewon KimLaboratory of Bio-informatics, Department of Multimedia Engineering, Dankook University, Cheonan 31116, Republic of Korea.
Adithan AravinthanDepartment of Physiology, College of Veterinary Medicine, Chonbuk National University, Iksan 54596, Republic of Korea.
Jong-Hoon KimDepartment of Physiology, College of Veterinary Medicine, Chonbuk National University, Iksan 54596, Republic of Korea.
Jae Youl ChoDepartment of Genetic Engineering, Sungkyunkwan University, Suwon 16419, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thymoquinone (TQ) is a bioactive component of black seed (Nigella sativa) volatile oil and has been shown to have anti-oxidative, anti-inflammatory, and anti-cancer properties. In the present study, we explored the molecular mechanisms that underlie the anti-inflammatory effect of TQ and its target proteins using lipopolysaccharide (LPS)-stimulated murine macrophage-like RAW264.7 and human monocyte-like U937 cells, together with LPS/D-galactosamine (GalN)-induced acute hepatitis and HCl/EtOH-induced gastritis mouse models. TQ strongly inhibited the production of nitric oxide (NO) and repressed NO synthase (iNOS), tumor necrosis factor (TNF)-α, cyclooxygenase (COX)-2, interleukin (IL)-6, and IL-1β expression in LPS-activated RAW264.7 cells. Treatment of LPS/D-GalN-induced hepatitis and EtOH/HCl-induced gastritis mouse models with TQ significantly ameliorated disease symptoms. Using luciferase reporter gene assays, we also showed that the nuclear levels of transcription factors and phosphorylation patterns of signaling proteins, activator protein (AP)-1, and nuclear factor (NF)-κB pathways were all affected by TQ treatment. Finally, we used additional kinase and luciferase validation assays with interleukin-1 receptor-associated kinase 1 (IRAK1) to show that IRAK1 is directly suppressed by TQ treatment. Together, these findings strongly suggest that the anti-inflammatory actions of TQ are caused by suppression of IRAK-linked AP-1/NF-κB pathways.

Indexed as

AnimalsAnti-Inflammatory AgentsBenzoquinonesCell LineCyclooxygenase 2GastritisGene Expression RegulationHumansInterleukin-1 Receptor-Associated KinasesLipopolysaccharidesMacrophagesMiceNF-kappa BNigella sativaNitric OxideNitric Oxide Synthase Type IIAnti-Inflammatory AgentsBenzoquinonesCyclooxygenase 2Interleukin-1 Receptor-Associated KinasesIRAK1 protein, humanLipopolysaccharidesNF-kappa BNitric OxideNitric Oxide Synthase Type IIthymoquinoneTranscription Factor AP-1Tumor Necrosis Factor-alpha

Identifiers

PMID28216638
PMCPMC5316937

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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.