Evidence map›Paper›PMID 25165413›Full record

ArticleMediators of inflammation2014

Paeonol attenuates cigarette smoke-induced lung inflammation by inhibiting ROS-sensitive inflammatory signaling.

Meng-Han Liu, An-Hsuan Lin, Hung-Fu Lee, Hsin-Kuo Ko, Tzong-Shyuan Lee, Yu Ru Kou

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.0field-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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Review
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  8. Article
  9. RBM3 is associated with acute lung injury in septic mice and patients via the NF-κB/NLRP3 pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  10. Review
  11. Plants (Basel, Switzerland) · 2022
    Review
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  14. Article
  15. StandardisedFrontiers in pharmacology · 2022
    Article
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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

6 authors at 2 institutions in 1 country.

Meng-Han LiuDepartment of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, Taiwan.ORCID 0000-0001-7550-2919
An-Hsuan LinDepartment of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, Taiwan.
Hung-Fu LeeDepartment of Neurosurgery, Cheng Hsin General Hospital, Taipei 11220, Taiwan.ORCID 0000-0002-9271-4478
Hsin-Kuo KoDepartment of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, Taiwan ; Department of Chest Medicine, Taipei Veterans General Hospital, Taipei 11217, Taiwan.
Tzong-Shyuan LeeDepartment of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, Taiwan.ORCID 0000-0002-9593-4062
Yu Ru KouDepartment of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, Taiwan.ORCID 0000-0002-4681-9009
National Yang Ming Chiao Tung University · TWCheng Hsin General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cigarette smoking causes persistent lung inflammation that is mainly regulated by redox-sensitive pathways. We have previously reported that cigarette smoke (CS) activates reactive oxygen species- (ROS-) sensitive mitogen-activated protein kinases (MAPKs)/nuclear factor-κB (NF-κB) signaling leading to induction of lung inflammation. Paeonol, the main phenolic compound present in the Chinese herb Paeonia suffruticosa, has antioxidant and anti-inflammatory properties. However, whether paeonol has similar beneficial effects against CS-induced lung inflammation remains unclear. Using a murine model, we showed that chronic CS exposure for 4 weeks caused pulmonary inflammatory infiltration, increased lung vascular permeability, elevated lung levels of chemokines, cytokines, and 4-hydroxynonenal (an oxidative stress biomarker), and induced lung inflammation; all of these CS-induced events were suppressed by chronic treatment with paeonol. Using human bronchial epithelial cells (HBECs), we demonstrated that cigarette smoke extract (CSE) sequentially increased extracellular and intracellular levels of ROS, activated the MAPKs/NF-κB signaling, and induced interleukin-8 (IL-8); all these CSE-induced events were inhibited by paeonol pretreatment. Our findings suggest a novel role for paeonol in alleviating the oxidative stress and lung inflammation induced by chronic CS exposure in vivo and in suppressing CSE-induced IL-8 in vitro via its antioxidant function and an inhibition of the MAPKs/NF-κB signaling.

Indexed as

AcetophenonesAnimalsAnti-Inflammatory AgentsBlotting, WesternCell LineCell SurvivalMaleMiceMice, Inbred C57BLPneumoniaReactive Oxygen SpeciesSignal TransductionSmokingAcetophenonesAnti-Inflammatory AgentspaeonolReactive Oxygen Species

Identifiers

PMID25165413
PMCPMC4137546
OpenAlexW2007591248

What OpenQuestion holds

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LicenceCC BY
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.