Evidence map›Paper›PMID 34799662›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2022

Vitamin E relieves chronic obstructive pulmonary disease by inhibiting COX2-mediated p-STAT3 nuclear translocation through the EGFR/MAPK signaling pathway.

Hui Zhao, Jiannan Gong, Lifang Li, Shuyin Zhi, Guang Yang, Pingping Li, Ruina Li, Jianqiang Li

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 27 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

8 authors at 1 institution in 1 country.

Hui ZhaoDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, PR China. hui_zhao@sxmu.edu.cn.
Jiannan GongDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, PR China.
Lifang LiDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, PR China.
Shuyin ZhiDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, PR China.
Guang YangDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, PR China.
Pingping LiDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, PR China.
Ruina LiDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, PR China.
Jianqiang LiDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, PR China.
Shanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with chronic obstructive pulmonary disease (COPD) are characterized by an imbalance between oxidant enzymes and antioxidant enzymes. In the present study, we explored the protective effect of vitamin E on COPD and the underlying mechanisms. Targets of vitamin E were predicted by bioinformatics analysis. After establishing cigarette smoke (CS)-induced COPD rats, the expression levels of epidermal growth factor receptor (EGFR), cyclooxygenase 2 (COX2), and transcriptional activity of signal transducer and activator of transcription 3 (STAT3) were measured. Additionally, the effects of vitamin E on CS-induced COPD were explored by assessing inflammation, the reactive oxygen species (ROS), the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA), viability of human bronchial epithelioid (HBE) cells, and the expression of EGFR/MAPK pathway-related factors after loss- and gain- function assays. Vitamin E alleviated COPD. Vitamin E inhibited MAPK signaling pathway through decreasing EGFR expression. Additionally, vitamin E suppressed CS-induced HBE cell damage. Functionally, vitamin E attenuated CS-induced inflammation, apoptosis, and ROS by inhibiting the EGFR/MAPK axis, thereby inhibiting COX2-mediated p-STAT3 nuclear translocation. Moreover, overexpression of COX2 attenuated the protective effect of vitamin E on COPD rats. The present study shows that vitamin E inhibits the expression of COX2 by negatively regulating the EGFR/MAPK pathway, thereby inhibiting the translocation of phosphorylated STAT3 to the nucleus and relieving COPD.

Indexed as

Active Transport, Cell NucleusAnimalsBronchiCell LineCell SurvivalCyclooxygenase 2Epithelial CellsErbB ReceptorsHumansMalondialdehydeMAP Kinase Signaling SystemPulmonary Disease, Chronic ObstructiveRatsReactive Oxygen SpeciesSTAT3 Transcription FactorSuperoxide DismutaseCyclooxygenase 2ErbB ReceptorsMalondialdehydeReactive Oxygen SpeciesSTAT3 Transcription FactorSuperoxide DismutaseVitamin EVitamins

Identifiers

PMID34799662
OpenAlexW3212193248

What OpenQuestion holds

Textmetadata
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.