Evidence map›Paper›PMID 25945076›Full record

ArticleJournal of inflammation (London, England)2015

Glucose 6-phosphate dehydrogenase knockdown enhances IL-8 expression in HepG2 cells via oxidative stress and NF-κB signaling pathway.

Hung-Chi Yang, Mei-Ling Cheng, Yi-Syuan Hua, Yi-Hsuan Wu, Hsin-Ru Lin, Hui-Ya Liu, Hung-Yao Ho, Daniel Tsun-Yee Chiu

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation (London, England), 2015. 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
0.8field-weighted citation impact, top 35% 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, 30 citations in OpenAlex.

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  7. Severity of oxidative stress as a hallmark in COVID-19 patients.European journal of medical research · 2023
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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.

Hung-Chi Yang *Healthy Aging Research Center, Chang Gung University, Kwei-Shan, Tao-Yuan 333 Taiwan.
Mei-Ling Cheng *Healthy Aging Research Center, Chang Gung University, Kwei-Shan, Tao-Yuan 333 Taiwan.
Yi-Syuan HuaDepartment of Medical Biotechnology and Laboratory Sciences, College of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 333 Taiwan.
Yi-Hsuan WuDepartment of Medical Biotechnology and Laboratory Sciences, College of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 333 Taiwan.
Hsin-Ru LinMolecular Medicine Research Center, College of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 333 Taiwan.
Hui-Ya LiuDepartment of Medical Biotechnology and Laboratory Sciences, College of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 333 Taiwan.
Hung-Yao HoDepartment of Medical Biotechnology and Laboratory Sciences, College of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 333 Taiwan.
Daniel Tsun-Yee ChiuHealthy Aging Research Center, Chang Gung University, Kwei-Shan, Tao-Yuan 333 Taiwan.
Chang Gung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study was designed to investigate the effect of glucose 6-phosphate dehydrogenase (G6PD) deficiency on pro-inflammatory cytokine secretion using a palmitate-induced inflammation HepG2 in vitro model. The modulation of cellular pro-inflammatory cytokine expression under G6PD deficiency during chronic hepatic inflammation has never been investigated before.

methodsThe culture medium of untreated and palmitate-treated G6PD-scramble (Sc) and G6PD-knockdown (Gi) HepG2 cells were subjected to cytokine array analysis, followed by validation with ELISA and qRT-PCR of the target cytokine. The mechanism of altered cytokine secretion in palmitate-treated Sc and Gi HepG2 cells was examined in the presence of anti-oxidative enzyme (glutathione peroxidase, GPX), anti-inflammatory agent (curcumin), NF-κB inhibitor (BAY11-7085) and specific SiRNA against NF-κB subunit p65.

resultsCytokine array analysis indicated that IL-8 is most significantly increased in G6PD-knockdown HepG2 cells. The up-regulation of IL-8 caused by G6PD deficiency in HepG2 cells was confirmed in other G6PD-deficient cells by qRT-PCR. The partial reduction of G6PD deficiency-derived IL-8 due to GPX and NF-κB blockers indicated that G6PD deficiency up-regulates pro-inflammatory cytokine IL-8 through oxidative stress and NF-κB pathway.

conclusionsG6PD deficiency predisposes cells to enhanced production of pro-inflammatory cytokine IL-8. Mechanistically, G6PD deficiency up-regulates IL-8 through oxidative stress and NF-κB pathway. The palmitate-induced inflammation in G6PD-deficient HepG2 cells could serve as an in vitro model to study the role of altered redox homeostasis in chronic hepatic inflammation.

Indexed as

AntioxidantG6PD deficiencyIL-8NF-κBOxidative stressPalmitatePro-inflammatory cytokine

Identifiers

PMID25945076
PMCPMC4419400
OpenAlexW2114077344

What OpenQuestion holds

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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.