Evidence map›Paper›PMID 27959438›Full record

ArticleMolecular medicine reports2017

Dexmedetomidine attenuates lipopolysaccharide-induced acute lung injury by inhibiting oxidative stress, mitochondrial dysfunction and apoptosis in rats.

Chunlai Fu, Xingui Dai, You Yang, Mengxiang Lin, Yeping Cai, Shaoxi Cai

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 98 citations in OpenAlex.

  1. Trial
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  3. Synergistic mitigation of endotoxin-induced liver injury by low-frequency PMF and 27.12 MHz RF-EMF: a multi-biomarker experimental study.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2026
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  15. Baicalin and lung diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

1 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 at 3 institutions in 1 country.

Chunlai FuChronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Xingui DaiDepartment of Critical Care Medicine, The First People's Hospital of Chenzhou, Institute of Translation Medicine, Chenzhou, Hunan 423000, P.R. China.
You YangMedical Imaging Center, The First People's Hospital of Chenzhou, Institute of Translation Medicine, Chenzhou, Hunan 423000, P.R. China.
Mengxiang LinDepartment of Critical Care Medicine, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Yeping CaiDepartment of Critical Care Medicine, The First People's Hospital of Chenzhou, Institute of Translation Medicine, Chenzhou, Hunan 423000, P.R. China.
Shaoxi CaiChronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Chenzhou First People's Hospital · CNSouthern Medical University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have identified that dexmedetomidine (DEX) treatment can ameliorate the acute lung injury (ALI) induced by lipopolysaccharide and ischemia-reperfusion. However, the molecular mechanisms by which DEX ameliorates lung injury remain unclear. The present study investigated whether DEX, which has been reported to exert effects on oxidative stress, mitochondrial permeability transition pores and apoptosis in other disease types, can exert protective effects in lipopolysaccharide (LPS)‑induced ALI by inhibiting oxidative stress, mitochondrial dysfunction and mitochondrial‑dependent apoptosis. It was revealed that LPS‑challenged rats exhibited significant lung injury, characterized by the deterioration of histopathology, vascular hyperpermeability, wet‑to‑dry weight ratio and oxygenation index (PaO2/FIO2), which was attenuated by DEX treatment. DEX treatment inhibited LPS‑induced mitochondrial dysfunction, as evidenced by alleviating the cellular ATP and mitochondrial membrane potential in vitro. In addition, DEX treatment markedly prevented the LPS‑induced mitochondrial‑dependent apoptotic pathway in vitro (increases of cell apoptotic rate, cytosolic cytochrome c, and caspase 3 activity) and in vivo (increases of |terminal deoxynucleotidyl transferase dUTP nick‑end labeling positive cells, cleaved caspase 3, Bax upregulation and Bcl‑2 downregulation). Furthermore, DEX treatment markedly attenuated LPS‑induced oxidative stress, as evidenced by downregulation of cellular reactive oxygen species in vitro and lipid peroxides in serum. Collectively, the present results demonstrated that DEX ameliorates LPS‑induced ALI by reducing oxidative stress, mitochondrial dysfunction and mitochondrial-dependent apoptosis.

Indexed as

Acute Lung InjuryAdrenergic alpha-2 Receptor AgonistsAnimalsAnti-Inflammatory AgentsApoptosisDexmedetomidineLipopolysaccharidesLungMaleMembrane Potential, MitochondrialMitochondriaOxidative StressRatsRats, Sprague-DawleyAdrenergic alpha-2 Receptor AgonistsAnti-Inflammatory AgentsDexmedetomidineLipopolysaccharides

Identifiers

PMID27959438
PMCPMC5355722
OpenAlexW2559861890

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.