Evidence map›Paper›PMID 29169345›Full record

ArticleBMC ophthalmology2017

The antioxidant effects of riluzole on the APRE-19 celll model injury-induced by t-BHP.

Chaolan Shen, Wei Ma, Wenbin Zheng, Hao Huang, Renchun Xia, Chu Li, Xiaobo Zhu

Open access · goldAbstract read
In one paragraph

Article in BMC ophthalmology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. 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

7 authors at 3 institutions in 1 country.

Chaolan ShenThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Wei MaThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Wenbin ZhengFrist Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, China.
Hao HuangThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Renchun XiaPeople's hospital of Deyang city, Deyang, Sichuan, China.
Chu LiThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Xiaobo ZhuThe State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China. zhuxbo@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-7158-2349
Sun Yat-sen University · CNDeyang Stomatological Hospital · CNFirst Affiliated Hospital of Gannan Medical University · CN

Funding

National Natural Science Foundation of China Grants 81271012Specialized Research Fund for the Doctoral Program of Higher Education of China 20100171120097
6 · The paper itself

Abstract

backgroundAge-related macular degeneration (AMD) causes the dysfunction of the retinal pigment epithelial (RPE) cells. In this study, we examined the effects of riluzole, a sustained activator of the TRAAK potassium channel, on human RPE (ARPE-19) cells in an oxidant-induced cell-injury model and elucidate the mechanism of riluzole on RPE cell apoptosis.

methodsThe follow four groups of ARPE-19 cells were treated with riluzole and/or tert-butyl hydroperoxide (t-BHP) for 24.0 h: control, t-BHP, riluzole, and t-BHP + riluzole. Cell apoptosis was measured by flow cytometry, and Western blotting was performed to analyze the expression of the weakly inward rectifying potassium (TRAAK) channel. Finally, the mitochondrial membrane potential (Δψm) was detected by flow cytometry, and cytochrome C (Cyt-c) release was assessed by Western blotting.

resultsThe viability of the cells in the cotreated group was significantly higher (85.6 ± 3.1%) than that in the t-BHP group (66.2 ± 2.5%). In addition, the cells in the cotreated group had a higher effect on increasing the expression of TRAAK than the t-BHP group. The results also showed that Cyt-c translocation significantly decreased and Δψm increased in the cotreated group.

conclusionsThese results demonstrate that riluzole protects RPE cells from apoptosis. The protection mechanism of riluzole could be from stabilizing mitochondrial Δψm and preventing the release of Cyt-c. Changes in TRAAK expression might also contribute to the protection of RPE cells.

Indexed as

AntioxidantsApoptosisCell SurvivalCytochromes cEpithelial CellsExcitatory Amino Acid AntagonistsHumansMacular DegenerationMembrane Potential, MitochondrialPotassium ChannelsRetinal Pigment EpitheliumRiluzoleAntioxidantsCytochromes cExcitatory Amino Acid AntagonistsKCNK4 protein, humanPotassium ChannelsRiluzoleAMDapoptosisARPE-19 cellsRiluzoleTRAAK K2P channel

Identifiers

PMID29169345
PMCPMC5701292
OpenAlexW2769796886

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.