Evidence map›Paper›PMID 28560453›Full record

ArticleMolecular medicine reports2017

Nrf2 mediates the protective effects of homocysteine by increasing the levels of GSH content in HepG2 cells.

Bing Zhang, Jing-Lin Dong, Ying-Li Chen, Yang Liu, Shi-Shun Huang, Xiu-Li Zhong, Yu-Hong Cheng, Zhi-Gang Wang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

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  13. TheFrontiers in immunology · 2018
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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

8 authors at 3 institutions in 1 country.

Bing ZhangCollege of Medical Laboratory Science and Technology, Harbin Medical University at Daqing, Daqing, Heilongjiang 163319, P.R. China.
Jing-Lin DongDaqing Oilfield General Hospital, Daqing, Heilongjiang 163001, P.R. China.
Ying-Li ChenCollege of Medical Laboratory Science and Technology, Harbin Medical University at Daqing, Daqing, Heilongjiang 163319, P.R. China.
Yang LiuCollege of Medical Laboratory Science and Technology, Harbin Medical University at Daqing, Daqing, Heilongjiang 163319, P.R. China.
Shi-Shun HuangCollege of Medical Laboratory Science and Technology, Harbin Medical University at Daqing, Daqing, Heilongjiang 163319, P.R. China.
Xiu-Li ZhongCollege of Medical Laboratory Science and Technology, Harbin Medical University at Daqing, Daqing, Heilongjiang 163319, P.R. China.
Yu-Hong ChengInspection Department, Daqing Medical College, Daqing, Heilongjiang 163311, P.R. China.
Zhi-Gang WangCollege of Medical Laboratory Science and Technology, Harbin Medical University at Daqing, Daqing, Heilongjiang 163319, P.R. China.
Daqing City People's Hospital · CNHarbin Medical University · CNDaqing Oilfield General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Homocysteine (Hcy) and glutathione (GSH) are crucial reduction‑oxidation mediators. The underlying mechanisms governing the effects of Hcy on GSH generation in the progression of alcoholic liver disease has so far received little attention. The present study hypothesized that the antioxidant transcriptional factor nuclear factor (erythroid‑derived 2)‑like 2 (Nrf2) may participate in Hcy‑mediated regulation of GSH production in HepG2 human liver cancer cells. MTT assay was used to study the cytotoxicity of homocysteine, western blot analysis and immunofluorescence staining were used to determine the effect of Hcy on Nrf2 expression. Our data demonstrated that HepG2 cells exposed to exogenous levels of Hcy (0‑100 µM) exhibited elevated GSH levels in a concentration‑dependent manner. Furthermore, 4‑hydroxynonenal (4‑HNE)‑induced cell injury was attenuated by Hcy; however, this protective effect was blocked by the GSH‑production inhibitor buthionine sulfoximine. Hcy treatment was able to induce Nrf2 protein expression in HepG2 cells. Treatment with the Nrf2 activator tert‑butylhydroquinone (0‑100 µM) increased GSH expression in a concentration‑dependent manner; however, Nrf2‑siRNA abolished the Hcy‑induced increase in GSH expression and cellular protection in 4‑HNE‑stressed HepG2 cells. In conclusion, the antioxidant transcriptional factor Nrf2 was demonstrated to mediate the Hcy‑induced increase in GSH expression levels and cellular protection in HepG2 cells.

Indexed as

AntioxidantsCell SurvivalGene Knockdown TechniquesGlutathioneHep G2 CellsHomocysteineHumansNF-E2-Related Factor 2Oxidation-ReductionOxidative StressProtective AgentsProtein TransportReactive Oxygen SpeciesAntioxidantsGlutathioneHomocysteineNF-E2-Related Factor 2Protective AgentsReactive Oxygen Species

Identifiers

PMID28560453
PMCPMC5482120
OpenAlexW2620414655

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.