Evidence map›Paper›PMID 28346481›Full record

ArticlePloS one2017

Edaravone protects against hyperosmolarity-induced oxidative stress and apoptosis in primary human corneal epithelial cells.

Yanwei Li, Haifeng Liu, Wei Zeng, Jing Wei

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.7field-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

31 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Targeting Nrf2 signaling in dry eye.International journal of ophthalmology · 2024
    Review
  8. Review
  9. Article
  10. Hyperosmolality in CHO cell culture: effects on the proteome.Applied microbiology and biotechnology · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Edaravone attenuates smoke inhalation injury in rats by the Notch pathway.American journal of translational research · 2021
    Article
  16. Demystifying Oxidative Stress.Handbook of experimental pharmacology · 2021
    Article
  17. Article
  18. Effects ofExperimental and therapeutic medicine · 2020
    Article
  19. Article
  20. Article
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

4 authors at 2 institutions in 1 country.

Yanwei LiDepartment of Ophthalmology, The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Haifeng LiuDepartment of Ophthalmology, The Third Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
Wei ZengDepartment of Otorhinolaryngology Head and Neck Surgery, The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Jing WeiDepartment of Ophthalmology, The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
First Affiliated Hospital of Henan University of Science and Technology · CNXinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An increase in the osmolarity of tears induced by excessive evaporation of the aqueous tear phase is a major pathological mechanism behind dry eye. Exposure of epithelial cells on the surface of the human eye to hyperosmolarity leads to oxidative stress, mitochondrial dysfunction, and apoptosis. Edaravone, a hydroxyl radical scavenging agent, is clinically used to reduce neuronal damage following ischemic stroke. In this study, we found that treatment with hyperosmotic media at 400 and 450 mOsM increased the levels of ROS and mitochondrial oxidative damage, which were ameliorated by edaravone treatment in a dose-dependent manner. We also found that edaravone could improve mitochondrial function in HCEpiCs by increasing the levels of ATP and mitochondrial membrane potential. MTT and LDH assays indicated that edaravone could attenuate hyperosmolarity-induced cell death. It was found that edaravone prevented apoptosis by decreasing the level of cleaved caspase-3, and attenuating the release of cytochrome C. Mechanistically, we found that edaravone augmented the expression of Nrf2 and its target genes, such as HO-1, GPx-1, and GCLC.

Indexed as

Adenosine TriphosphateAntipyrineApoptosisCaspase 3EdaravoneEpithelial CellsEpithelium, CornealFree Radical ScavengersHumansMembrane Potential, MitochondrialMitochondriaOsmolar ConcentrationOxidative StressProtective AgentsReactive Oxygen SpeciesAdenosine TriphosphateAntipyrineCaspase 3EdaravoneFree Radical ScavengersProtective AgentsReactive Oxygen Species

Identifiers

PMID28346481
PMCPMC5367814
OpenAlexW2599672684

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.