Evidence map›Paper›PMID 28128352›Full record

ArticleScientific reports2017

Astaxanthin protects against early burn-wound progression in rats by attenuating oxidative stress-induced inflammation and mitochondria-related apoptosis.

Quan Fang, Songxue Guo, Hanlei Zhou, Rui Han, Pan Wu, Chunmao Han

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 114 citations in OpenAlex.

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  4. [Research progress on the roles of mitochondrial fusion, fission, and mitophagy in burn wound healing​].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
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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.

Quan FangDepartment of Burns, Second Affiliated Hospital, Zhejiang University, College of Medicine, 88 Jiefang Road, Hangzhou 310009, Zhejiang, China.
Songxue GuoDepartment of Burns, Second Affiliated Hospital, Zhejiang University, College of Medicine, 88 Jiefang Road, Hangzhou 310009, Zhejiang, China.
Hanlei ZhouDepartment of Burns, Second Affiliated Hospital, Zhejiang University, College of Medicine, 88 Jiefang Road, Hangzhou 310009, Zhejiang, China.
Rui HanDepartment of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, 3 East Qingchun Road, Hangzhou 310020, Zhejiang, China.
Pan WuDepartment of Burns, Second Affiliated Hospital, Zhejiang University, College of Medicine, 88 Jiefang Road, Hangzhou 310009, Zhejiang, China.
Chunmao HanDepartment of Burns, Second Affiliated Hospital, Zhejiang University, College of Medicine, 88 Jiefang Road, Hangzhou 310009, Zhejiang, China.
Second Affiliated Hospital of Zhejiang University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Burn-wound progression can occur in the initial or peri-burn area after a deep burn injury. The stasis zone has a higher risk of deterioration mediated by multiple factors but is also considered salvageable. Astaxanthin (ATX), which is extracted from some marine organisms, is a natural compound with a strong antioxidant effect that has been reported to attenuate organ injuries caused by traumatic injuries. Hence, we investigated the potential effects of ATX on preventing early burn-wound progression. A classic "comb" burn rat model was established in this study for histological and biological assessments, which revealed that ATX, particularly higher doses, alleviated histological deterioration in the stasis zone. Additionally, we observed dose-dependent improvements in oxidative stress and the release of inflammatory mediators after ATX treatment. Furthermore, ATX dose-dependently attenuated burn-induced apoptosis in the wound areas, and this effect was accompanied by increases in Akt and Bad phosphorylation and a downregulation of cytochrome C and caspase expression. In addition, the administration of Ly 294002 further verified the effect of ATX. In summary, we demonstrated that ATX protected against early burn-wound progression in a rat deep-burn model. This protection might be mediated by the attenuation of oxidative stress-induced inflammation and mitochondria-related apoptosis.

Indexed as

ApoptosisDisease ProgressionOxidative StressAnimalsbcl-Associated Death ProteinBurnsChromonesInflammationInflammation MediatorsMaleMitochondriaModels, BiologicalMorpholinesPhosphorylationProtective AgentsProto-Oncogene Proteins c-akt2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneastaxanthinebcl-Associated Death ProteinChromonesInflammation MediatorsMorpholinesProtective AgentsProto-Oncogene Proteins c-aktXanthophylls

Identifiers

PMID28128352
PMCPMC5269753
OpenAlexW2581671813

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.