Evidence map›Paper›PMID 28586068›Full record

ArticleMolecular medicine reports2017

Sulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract.

Zongxian Jiao, Jiachen Chang, Jing Li, Dengmei Nie, Huijuan Cui, Dongfang Guo

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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

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  18. Why new biology must be uncovered to advance therapeutic strategies for chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2021
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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

6 authors at 1 institution in 1 country.

Zongxian JiaoResearch Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Jiachen ChangResearch Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Jing LiResearch Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Dengmei NieResearch Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Huijuan CuiResearch Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Dongfang GuoResearch Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Lanzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cigarette smoking is a primary risk factor for chronic obstructive pulmonary disease (COPD), as it damages epithelial cells through a variety of mechanisms. Sulforaphane (SFN) is an antioxidant agent, which exerts protective effects against cell damage by activating the nuclear factor erythroid 2 like 2 (NFE2L2; Nrf2). The present study was undertaken to investigate the effects and underlying mechanisms of SFN in preventing cigarette smoke extract (CSE)‑induced oxidative damage to RLE‑6TN rat lung epithelial cells. MTT assay was used to determine the cytotoxicity of SFN and CSE. The effect of SFN and CSE on cell cycle progression, apoptosis and intracellular reactive oxygen species (ROS) levels were analyzed using flow cytometry. Reverse transcription‑quantitative polymerase chain reaction and western blotting were used to quantify mRNA and protein expression levels of Nrf2 respectively. SFN protected RLE‑6TN cells from oxidative damage, potentially via increasing Nrf2 expression and reducing ROS levels. In addition, SFN attenuated G1 phase cell cycle arrest and abrogated apoptosis. Therefore, SFN protected alveolar epithelial cells against CSE‑induced oxidative injury by upregulating Nrf2 expression. The results of the present study may provide theoretical support for the clinical use of SFN in patients with COPD.

Indexed as

Alveolar Epithelial CellsAnimalsApoptosisCell CycleCell LineCell SurvivalDose-Response Relationship, DrugGene Expression RegulationIsothiocyanatesNF-E2-Related Factor 2NicotianaOxidative StressProtective AgentsPulmonary Disease, Chronic ObstructiveRatsReactive Oxygen SpeciesIsothiocyanatesNF-E2-Related Factor 2Protective AgentsReactive Oxygen SpeciesRNA, MessengersulforaphaneSulfoxides

Identifiers

PMID28586068
PMCPMC5562053
OpenAlexW2624371671

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.