Evidence map›Paper›PMID 37509477›Full record

ArticleBiomedicines2023

The Potential of Glucose Treatment to Reduce Reactive Oxygen Species Production and Apoptosis of Inflamed Neural Cells In Vitro.

Juin-Hong Cherng, Shu-Jen Chang, Hsin-Da Tsai, Chung-Fang Chun, Gang-Yi Fan, Kenneth Dean Reeves, King Hei Stanley Lam, Yung-Tsan Wu

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2023. 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
3.9field-weighted citation impact, top 6% 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, 22 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 5 institutions in 3 countries.

Juin-Hong CherngGraduate Institute of Life Sciences, National Defense Medical Center, Taipei 11490, Taiwan.ORCID 0000-0002-7722-6134
Shu-Jen ChangDepartment and Graduate Institute of Biology and Anatomy, National Defense Medical Center, Taipei 11490, Taiwan.ORCID 0000-0001-6203-057X
Hsin-Da TsaiLaboratory of Adult Stem Cell and Tissue Regeneration, National Defense Medical Center, Taipei 11490, Taiwan.ORCID 0000-0002-8991-6343
Chung-Fang ChunGraduate Institute of Life Sciences, National Defense Medical Center, Taipei 11490, Taiwan.
Gang-Yi FanDepartment and Graduate Institute of Biology and Anatomy, National Defense Medical Center, Taipei 11490, Taiwan.
Kenneth Dean ReevesPrivate Practice PM&R and Pain Management, Roeland Park, KS 66205, USA.ORCID 0000-0002-2346-2326
King Hei Stanley LamThe Hong Kong Institute of Musculoskeletal Medicine, Hong Kong.ORCID 0000-0003-1392-829X
Yung-Tsan WuDepartment of Physical Medicine and Rehabilitation, Tri-Service General Hospital, School of Medicine, National Defense Medical Center, Taipei 11490, Taiwan.ORCID 0000-0003-1175-7909
National Defense Medical Center · TWChinese University of Hong Kong · HKChung Yuan Christian University · TWPain Management Institute · USTri-Service General Hospital · TW

Funding

National Science and Technology Council NSTC 111-2314-B-016-029Tri-service general hospital TSGH-E-112248
6 · The paper itself

Abstract

Neuroinflammation is a key feature in the pathogenesis of entrapment neuropathies. Clinical trial evidence suggests that perineural injection of glucose in water at entrapment sites has therapeutic benefits beyond a mere mechanical effect. We previously demonstrated that 12.5-25 mM glucose restored normal metabolism in human SH-SYFY neuronal cells rendered metabolically inactive from TNF-α exposure, a common initiator of neuroinflammation, and reduced secondary elevation of inflammatory cytokines. In the present study, we measured the effects of glucose treatment on cell survival, ROS activity, gene-related inflammation, and cell cycle regulation in the presence of neurogenic inflammation. We exposed SH-SY5Y cells to 10 ng/mL of TNF-α for 24 h to generate an inflammatory environment, followed by 24 h of exposure to 3.125, 6.25, 12.5, and 25 mM glucose. Glucose exposure, particularly at 12.5 mM, preserved apoptotic SH-SY5Y cell survival following a neuroinflammatory insult. ROS production was substantially reduced, suggesting a ROS scavenging effect. Glucose treatment significantly increased levels of CREB, JNK, and p70S6K (

Indexed as

cell cycleglucosein vitroneural cellneuroinflammationreactive oxygen speciestreatment

Identifiers

PMID37509477
PMCPMC10376532
OpenAlexW4382278945

What Socratic 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 Socratic graph.