Evidence map›Paper›PMID 28212544›Full record

ArticleOncotarget2017

Protective effect of DHEA on hydrogen peroxide-induced oxidative damage and apoptosis in primary rat Leydig cells.

Xiao Ding, Lei Yu, Chongyang Ge, Haitian Ma

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

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 1 institution in 1 country.

Xiao DingKey Laboratory of Animal Physiology and Biochemistry, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Lei YuKey Laboratory of Animal Physiology and Biochemistry, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Chongyang GeKey Laboratory of Animal Physiology and Biochemistry, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Haitian MaKey Laboratory of Animal Physiology and Biochemistry, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Nanjing Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dehydroepiandrosterone (DHEA) is widely used as a nutritional supplement due to its putative anti-aging properties. However, the effect of DHEA in Leydig cells, a major target cell of DHEA biotransformation in male, are not clear. The present study aimed to investigate the preventative effect of DHEA on oxidative damage and apoptosis after H2O2 treatment in Leydig cells. The results showed that DHEA treatment attenuated the reduction of cell viability induced by H2O2. No differences were observed on the superoxide anion (O2-) content, while DHEA treatment decreased reactive oxygen species (ROS) and hydroxyl radical (•OH) content in H2O2-treated Leydig cells. Pre-treatment with DHEA increased peroxidase (POD) activity and decreased glutathione peroxidase (GSH-Px) activity in H2O2-treated Leydig cell. DHEA treatment attenuated DNA damage as indicated by the decreasing of tail moment, comet length and olive tail moment. Total apoptosis ratio and early apoptosis ratio were significantly decreased in H2O2-treated Leydig cell that were pre-treatment with DHEA. DHEA treatment decreased Bax, capase-9 and capase-3 mRNA levels in H2O2-treated Leydig cells. Our results demonstrated that pre-treatment with DHEA prevented the Leydig cells oxidative damage caused by H2O2 through increasing POD activity, which resulted in inhibition of •OH generation. Meanwhile, pre-treatment with DHEA inhibited H2O2-induced Leydig cells early apoptosis which mainly by reducing the pro-apoptotic protein Bax and caspases-9, caspases-3 mRNA levels. This information is important to understand the molecular mechanism of anti-ageing effect and potential application in treatment of oxidative stress induced related diseases of DHEA.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinCaspase 3Cells, CulturedCell SurvivalComet AssayDehydroepiandrosteroneDNA DamageGene ExpressionGlutathione PeroxidaseHydrogen PeroxideLeydig CellsMaleMalondialdehydeOxidantsBax protein, ratbcl-2-Associated X ProteinCaspase 3DehydroepiandrosteroneGlutathione PeroxidaseHydrogen PeroxideMalondialdehydeOxidantsPeroxidaseProtective AgentsReactive Oxygen SpeciesTestosteroneapoptosisdehydroepiandrosteroneLeydig cellsoxidative damagePathology Section

Identifiers

PMID28212544
PMCPMC5369954
OpenAlexW2588738454

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.