Evidence map›Paper›PMID 27009328›Full record

ArticleJournal of translational medicine2016

Resolvin D1 mitigates energy metabolism disorder after ischemia-reperfusion of the rat lung.

Qifeng Zhao, Ji Wu, Qingwang Hua, Zhiyong Lin, Leping Ye, Weixi Zhang, Guowei Wu, Jie Du, Jie Xia, Maoping Chu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

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  18. Does methylene blue attenuate inflammation in nonischemic lungs after lung transplantation?Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia
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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

11 authors at 3 institutions in 1 country.

Qifeng ZhaoThe Department of Children's Cardiovascular and Thoracic Surgery, Children's Heart Center, the Second Affiliated Hospital, Yuying Children's Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, 325000, Wenzhou, People's Republic of China.
Ji WuWuhan Medical & Healthcare Center for Woman and Children, 430015, Wuhan, People's Republic of China.
Qingwang HuaThe Department of Children's Cardiovascular and Thoracic Surgery, Children's Heart Center, the Second Affiliated Hospital, Yuying Children's Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, 325000, Wenzhou, People's Republic of China.
Zhiyong LinThe Department of Children's Cardiovascular and Thoracic Surgery, Children's Heart Center, the Second Affiliated Hospital, Yuying Children's Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, 325000, Wenzhou, People's Republic of China.
Leping YeThe Department of Children's Respiration Medicine, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, 325000, Wenzhou, People's Republic of China.
Weixi ZhangThe Department of Children's Respiration Medicine, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, 325000, Wenzhou, People's Republic of China.
Guowei WuThe Department of Children's Cardiovascular and Thoracic Surgery, Children's Heart Center, the Second Affiliated Hospital, Yuying Children's Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, 325000, Wenzhou, People's Republic of China.
Jie DuThe Department of Children's Cardiovascular and Thoracic Surgery, Children's Heart Center, the Second Affiliated Hospital, Yuying Children's Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, 325000, Wenzhou, People's Republic of China.
Jie XiaThe Department of Children's Cardiovascular and Thoracic Surgery, Children's Heart Center, the Second Affiliated Hospital, Yuying Children's Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, 325000, Wenzhou, People's Republic of China.
Maoping ChuThe Department of Children's Cardiovascular Medicine, Children's Heart Center, the Second Affiliated Hospital, Yuying Children's Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, 325000, Wenzhou, People's Republic of China.
Xingti HuThe Department of Children's Cardiovascular and Thoracic Surgery, Children's Heart Center, the Second Affiliated Hospital, Yuying Children's Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, 325000, Wenzhou, People's Republic of China. huxingti@126.com.
Wenzhou Medical University · CNSecond Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University · CNWuhan Medical Center for Women and Children · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEnergy metabolism disorder is a critical process in lung ischemia-reperfusion injury (LIRI). This study was aimed to determine the effects of resolvin D1 (RvD1) on the energy metabolism in LIRI.

methodsForty Sprague-Dawley rats were divided into the following groups: Sham group; untreated ischemia-reperfusion (IR) control; IR treated with normal saline (IR-NS); and IR treated with RvD1 (IR-RV) (100 μg/kg, iv). LIRI and energy metabolism disorder were determined in these rats.

resultsThe results revealed that the levels of interleukin (IL)-1β, tumor necrosis factor-α, IL-10, monocyte chemoattractant protein-1, macrophage inflammatory protein-2, cytokine-induced neutrophil chemoattractant-1, injured alveoli rate, apoptosis index, pulmonary permeability index, malondialdehyde, ADP, and lactic acid were increased, whereas the levels of ATP, ATP/ADP, glycogen, Na(+)-K(+)-ATPase, superoxide dismutase, glutathione peroxidase activity, pulmonary surfactant associated protein-A, and oxygenation index were decreased in rats with LIRI. Except for IL-10, all these biomarkers of LIRI and its related energy metabolism disorder were significantly inhibited by RvD1 treatment. In addition, histological analysis via hematoxylin-eosin staining, and transmission electron microscopy confirmed that IR-induced structure damages of lung tissues were reduced by RvD1.

conclusionRvD1 improves the energy metabolism of LIRI disturbance, protects the mitochondrial structure and function, increases the ATP, glycogen content and Na(+)-K(+)-ATPase activity of lung tissue, balances the ratio of ATP/ADP and finally decreases the rate of apoptosis, resulting in the protection of IR-induced lung injury. The improved energy metabolism after LIRI may be related to the reduced inflammatory response, the balance of the oxidative/antioxidant and the pro-inflammatory/anti-inflammatory systems in rats.

Indexed as

AnimalsApoptosisDocosahexaenoic AcidsEnergy MetabolismInflammationLungLung InjuryMaleOxidative StressRats, Sprague-DawleyReperfusion InjuryRespiratory Function TestsDocosahexaenoic Acidsresolvin D1Energy metabolismInflammatory factorLung ischemia/reperfusion injuryOxidative stressResolvin

Identifiers

PMID27009328
PMCPMC4806414
OpenAlexW2311862640

What OpenQuestion holds

Textmetadata
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.