Evidence map›Paper›PMID 29497773›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2018

Luteolin activates ERK1/2- and Ca

Eun Jung Park, Young Min Kim, Hye Jung Kim, Ki Churl Chang

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 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
4.1field-weighted citation impact, top 6% 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, 61 citations in OpenAlex.

  1. Review
  2. ERK1/2 activation in anti-inflammatory effects and underlying signaling mechanisms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Immunopharmacological Activities of Luteolin in Chronic Diseases.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Proteomic analysis and identification reveal the anti-inflammatory mechanism of clofazimine on lipopolysaccharide-induced acute lung injury in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Cyclooxygenase-2 deficiency attenuates lipopolysaccharide-induced inflammation, apoptosis, and acute lung injury in adult mice.American journal of physiology. Regulatory, integrative and comparative physiology · 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

4 authors at 1 institution in 1 country.

Eun Jung ParkDepartment of Pharmacology and Institute of Health Sciences, School of Medicine, Gyeongsang National University, Jinju, 52527, Republic of Korea.
Young Min KimDepartment of Pharmacology and Institute of Health Sciences, School of Medicine, Gyeongsang National University, Jinju, 52527, Republic of Korea.
Hye Jung KimDepartment of Pharmacology and Institute of Health Sciences, School of Medicine, Gyeongsang National University, Jinju, 52527, Republic of Korea.
Ki Churl ChangDepartment of Pharmacology and Institute of Health Sciences, School of Medicine, Gyeongsang National University, Jinju, 52527, Republic of Korea. kcchang@gnu.kr.
Gyeongsang National University · KR

Funding

National Research Foundation of Korea (NRF) grant 2016R1A2B4008471
6 · The paper itself

Abstract

objectiveAlthough luteolin has shown to have anti-inflammatory action, no report is available whether luteolin inhibits HMGB1 and protects acute lung injury (ALI) in endotoxin rodents. We hypothesized that HO-1 induction by luteolin might play a crucial role for inhibition of pro-inflammatory mediators including HMGB1 through MAPK signaling in LPS-induced RAW264.7 cells, and it ameliorates ALI of endotoxin mice.

methodsThe effects of luteolin on the production of pro-inflammatory mediators in LPS-activated RAW264.7 cells and LPS-injected mice were evaluated. The mechanisms were investigated using various signal inhibitors.

resultsLuteolin significantly increased HO-1 expression through ERK1/2 signaling in a time- and concentration-dependent manner. Indeed, luteolin inhibited pro-inflammatory mediators (HMGB1, iNOS/NO, COX-2, and NF-κB activity) in LPS-activated RAW264.7 cells. In addition, PD98059, an ERK1/2 inhibitor, treatment failed to inhibit production of these pro-inflammatory mediators by luteolin. Interestingly, luteolin augmented HO-1 induction through Ca

conclusionTherefore, we conclude that luteolin has a great potential for treatment of ALI and related diseases, where HMGB1 is a therapeutic target.

Indexed as

Acute Lung InjuryAnimalsCalcium SignalingCell SurvivalCyclooxygenase 2EndotoxinsHeme Oxygenase-1HMGB1 ProteinLipopolysaccharidesLuteolinMaleMAP Kinase Signaling SystemMiceMice, Inbred BALB CNitric Oxide Synthase Type IIRAW 264.7 CellsCyclooxygenase 2EndotoxinsHeme Oxygenase-1HMGB1 ProteinHMGB1 protein, mouseLipopolysaccharidesLuteolinNitric Oxide Synthase Type IINos2 protein, mousePtgs2 protein, mouseAcute lung injuryHeme oxygenaseHMGB1InflammationSepsis

Identifiers

PMID29497773
OpenAlexW2790632158

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.