Evidence map›Paper›PMID 26143291›Full record

ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2015

Inhibition of p38 mitogen-activated protein kinase phosphorylation decreases H₂O₂-induced apoptosis in human lens epithelial cells.

Jie Bai, Yi Zheng, Li Dong, Xuehui Cai, Gang Wang, Ping Liu

Erratum issuedAbstract read
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In one paragraph

Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Jie BaiEye Hospital, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Road, Harbin, People's Republic of China.
Yi ZhengEye Hospital, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Road, Harbin, People's Republic of China.
Li DongEye Hospital, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Road, Harbin, People's Republic of China.
Xuehui CaiState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, People's Republic of China.
Gang WangState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, People's Republic of China.
Ping LiuEye Hospital, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Road, Harbin, People's Republic of China. cao770717@163.com.
First Affiliated Hospital of Harbin Medical University · CNChinese Academy of Agricultural Sciences · CNHarbin Veterinary Research Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOxidative damage resulting from ROS is a known causal factor for cataractogenesis. The mitogen-activated protein kinases (MAPK) pathway plays an important role in the apoptosis of HLE cells. The purpose of this study was to investigate the role of phosphorylated p38 mitogen-activated protein kinase in H2O2-induced apoptosis in cultured human lens epithelial (HLE) cells.

methodsThe effect of SB203580 on HLE cells treated with H2O2 was determined by various assays. Cell viability was monitored by the MTT assay. The rates of apoptosis and ROS generation were determined by flow cytometric analysis. The numbers of mitotic and apoptotic cell nuclei were determined after staining with Hoechst 33342. The protein level of phospho-p38 was measured using western blot analysis.

resultsSB203580 reduced H2O2-induced cellular apoptosis and inhibited the generation of reactive oxygen species (ROS); it also delayed the progression of H2O2-induced opacification of lenses. The level of p-p38 was increased when cells were exposed to H2O2 and significantly SB203580-inhibited phosphorylation of p38. The p38MAPK pathway plays an important role in H2O2-induced apoptosis of HLE cells.

conclusionsThe study demonstrates that activation of p38MAPK plays an important role in H2O2-induced apoptosis of HLE cells. SB203580 may potentially be exploited as a useful tool for cataract prevention.

Indexed as

AnimalsApoptosisBlotting, WesternCells, CulturedCell SurvivalEnzyme InhibitorsEpithelial CellsFlow CytometryHumansHydrogen PeroxideImidazolesLens, CrystallineMaleOxidantsOxidative Stressp38 Mitogen-Activated Protein KinasesEnzyme InhibitorsHydrogen PeroxideImidazolesOxidantsp38 Mitogen-Activated Protein KinasesPyridinesReactive Oxygen SpeciesSB 203580ApoptosisHuman lens epithelial cellsSB203580

Identifiers

PMID26143291
OpenAlexW4240170103

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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.