Evidence map›Paper›PMID 30838902›Full record

ArticleMolecular pain

Downregulation of glucose-6-phosphate dehydrogenase contributes to diabetic neuropathic pain through upregulation of toll-like receptor 4 in rats.

Qian Sun, Bing-Yu Zhang, Ping-An Zhang, Ji Hu, Hong-Hong Zhang, Guang-Yin Xu

Open access · goldAbstract read
In one paragraph

Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  16. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
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  17. TIGAR Attenuates High Glucose-Induced Neuronal ApoptosisFrontiers in molecular neuroscience · 2019
    Article
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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 2 institutions in 1 country.

Qian Sun1 Department of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, P. R. China.
Bing-Yu Zhang1 Department of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, P. R. China.
Ping-An Zhang2 Center for Translational Pain Medicine, Institute of Neuroscience, Soochow University, Suzhou, P. R. China.
Ji Hu1 Department of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, P. R. China.
Hong-Hong Zhang1 Department of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, P. R. China.
Guang-Yin Xu2 Center for Translational Pain Medicine, Institute of Neuroscience, Soochow University, Suzhou, P. R. China.
Soochow University · CNSecond Affiliated Hospital of Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimDiabetic neuropathic pain is a refractory and disabling complication of diabetes mellitus. The pathogenesis of the diabetic neuropathic pain is still unclear, and treatment is insufficient. The aim of this study is to investigate the roles of glucose-6-phosphate dehydrogenase (G6PD) and toll-like receptor 4 (TLR4) in neuropathic pain in rats with diabetes.

methodsType 1 diabetes model was induced by intraperitoneal injection of streptozotocin (STZ, 75 mg/kg) in adult female Sprague-Dawley rats. Paw withdrawal threshold and paw withdrawal latency of rats were measured by von Frey filaments and thermal radiation, respectively. The expressions of G6PD and TLR4 in L4-L6 dorsal root ganglions (DRGs) were measured by western blotting and quantitative real-time polymerase chain reaction analysis. Fluorescent immunohistochemistry was employed to detect expressions of G6PD and TLR4 and co-location of G6PD with TLR4.

resultsThe mRNA and protein expression levels of G6PD in DRGs were significantly decreased in diabetic rats when compared with age-matched control rats. Upregulation of G6PD by intrathecal injection of G6PD overexpression adenovirus markedly attenuated hindpaw pain hypersensitivity of diabetic rats. The mRNA and protein expression levels of TLR4 in DRGs of diabetic rats were significantly increased when compared with control rats. Intrathecal injection of TLR4-selective inhibitor CLI-095 attenuated diabetic pain in dose- and time-dependent manners. Furthermore, G6PD and TLR4 were co-localized in DRG neurons. Intrathecal injection of G6PD overexpression adenovirus greatly reduced TLR4 expression, while intrathecal injection of CLI-095 had no significant effect on G6PD expression in diabetic rats.

conclusionsOur results suggest that decrease in G6PD expression was involved in diabetic peripheral neuropathic pain, which was most likely through upregulation of TLR4 expression in the DRGs of rats.

Indexed as

AnimalsDiabetic NeuropathiesFemaleGanglia, SpinalGlucosephosphate DehydrogenaseRatsRats, Sprague-DawleySignal TransductionSulfonamidesToll-Like Receptor 4ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylateGlucosephosphate DehydrogenaseSulfonamidesToll-Like Receptor 4Diabetesdorsal root ganglionglucose-6-phosphate dehydrogenaseneuropathic paintoll-like receptor 4

Identifiers

PMID30838902
PMCPMC6487759
OpenAlexW2921263439

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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.