Evidence map›Paper›PMID 29599805›Full record

ArticleEvidence-based complementary and alternative medicine : eCAM2018

Qi-Dong-Huo-Xue-Yin Inhibits Inflammation in Acute Lung Injury in Mice via Toll-Like Receptor 4/Caveolin-1 Signaling.

Li-Ying Xu, Wan-Ru Cai, Chun-Fang Ma, Qi-Yang Shou, Jing-Li Qian, Turan S Huseyin

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Evidence-based complementary and alternative medicine : eCAM, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Li-Ying XuDepartment of Emergency, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.ORCID 0000-0001-8238-106X
Wan-Ru CaiDepartment of Respiratory Medicine, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.ORCID 0000-0002-8810-1548
Chun-Fang MaDepartment of Laboratory Medicine, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
Qi-Yang ShouAnimal Experimental Center, Zhejiang Chinese Medical University, Hangzhou, China.ORCID 0000-0003-1615-5309
Jing-Li QianDepartment of Respiratory Medicine, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
Turan S HuseyinAccident and Emergency Department, Royal Free London NHS Foundation Trust, London, UK.
Zhejiang Chinese Medical University · CNRoyal Free London NHS Foundation Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute lung injury (ALI) is a critical illness with no current effective treatment. Caveolin-1 indirectly activates inflammation-associated signaling pathways by inhibiting endothelial nitric oxide synthase (eNOS). This induces an imbalance between pro- and anti-inflammatory cytokine levels, which are involved in the pathogenesis of ALI. The compound Chinese prescription Qi-Dong-Huo-Xue-Yin (QDHXY) is efficacious for ALI treatment via an anti-inflammatory effect; however, the exact underlying mechanism is unknown. Therefore, we explored the protective effect of QDHXY against lipopolysaccharide- (LPS-) induced ALI in mice. Histopathological changes in mouse lung tissues were studied. Furthermore, alterations in the serum levels of pro- and anti-inflammatory cytokines were investigated. The levels of tumor necrosis factor- (TNF-)

Identifiers

PMID29599805
PMCPMC5827893
OpenAlexW2787467958

What OpenQuestion holds

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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.