Evidence map›Paper›PMID 20348278›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010

Identification of triptolide, a natural diterpenoid compound, as an inhibitor of lung inflammation.

Gary W Hoyle, Christine I Hoyle, Jing Chen, Weiyuan Chang, Ronald W Williams, Roy J Rando

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
19.6field-weighted citation impact, top 1% 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

32 citing papers in PubMed, 64 citations in OpenAlex.

  1. Trial
  2. Article
  3. A worldwide bibliometric analysis of triptolide research from 1997 to 2021.American journal of translational research · 2022
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  17. Abnormal epithelial structure and chronic lung inflammation after repair of chlorine-induced airway injury.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  18. 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 3 institutions in 1 country.

Gary W HoyleDepartment of Environmental and Occupational Health Sciences, School of Public Health and Information Sciences, University of Louisville, Louisville, KY 40202, USA. Gary.Hoyle@louisville.edu
Christine I Hoyle
Jing Chen
Weiyuan Chang
Ronald W Williams
Roy J Rando
University of Louisville · USTulane University · USVirginia Commonwealth University Medical Center · US

Funding

Novel Therapies for Chlorine-Induced Lung InjuryU01ES015673 · NIEHS · UNIVERSITY OF LOUISVILLE · PI HOYLE, GARY W. · 2006 to 2015
$4.6M
NIEHS NIH HHS U01 ES-015673NIEHS NIH HHS U01 ES015673
6 · The paper itself

Abstract

Inflammation is associated with various pulmonary diseases and contributes to the pathogenesis of acute lung injury. We previously identified a proinflammatory signaling pathway triggered by G protein-coupled receptors (GPCRs) in which stimulation of G(q)-coupled GPCRs results in activation of the transcription factor NF-kappaB. Because damage to the lung causes the release of multiple mediators acting through G(q)-coupled GPCRs, this signaling pathway is likely to contribute to inflammatory processes in the injured lung. In an effort to identify novel inhibitors of lung inflammation, the National Institutes of Health Clinical Collection, a library of 446 compounds, was screened for inhibitory activity toward production of IL-8 induced by stimulation of the G(q)-coupled tachykinin 1 receptor with substance P in A549 cells. Twenty-eight compounds that significantly inhibited substance P-induced IL-8 production were identified. The most potent inhibitor was triptolide, a diterpenoid compound from Tripterygium wilfordii Hook F, a vine used in traditional Chinese medicine for the treatment of autoimmune diseases. Triptolide inhibited IL-8 production induced by substance P with an IC(50) of 2.3 x 10(-8) M and inhibited NF-kappaB activation in response to an agonist of the protease-activated receptor 2 with an IC(50) of 1.4 x 10(-8) M. Anti-inflammatory effects of triptolide were assessed in vivo using a chlorine gas lung injury model in mice. Triptolide inhibited neutrophilic inflammation and the production of KC (Cxcl1) in the lungs of chlorine-exposed mice. The results demonstrate that triptolide exhibits anti-inflammatory activity in cultured lung cells and in an in vivo model of acute lung injury.

Indexed as

AnimalsAnti-Inflammatory AgentsCell Line, TumorChlorineDiterpenesEpoxy CompoundsHumansInterleukin-8LungMiceNF-kappa BPhenanthrenesPneumoniaSubstance PAnti-Inflammatory AgentsChlorineDiterpenesEpoxy CompoundsInterleukin-8NF-kappa BPhenanthrenesSubstance Ptriptolide

Identifiers

PMID20348278
PMCPMC2886612
OpenAlexW2018937158

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.