Evidence map›Paper›PMID 39457659›Full record

ArticleBiomedicines2024

Intestinal Region-Dependent Impact of NFκB-Nrf Crosstalk in Myenteric Neurons and Adjacent Muscle Cells in Type 1 Diabetic Rats.

Bence Pál Barta, Benita Onhausz, Abigél Egyed-Kolumbán, Afnan Al Doghmi, János Balázs, Zita Szalai, Ágnes Ferencz, Edit Hermesz, Mária Bagyánszki, Nikolett Bódi

Abstract read
In one paragraph

Article in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

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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

10 authors.

Bence Pál BartaDepartment of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, 6726 Szeged, Hungary.ORCID 0000-0002-5309-8633
Benita OnhauszDepartment of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, 6726 Szeged, Hungary.
Abigél Egyed-KolumbánDepartment of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, 6726 Szeged, Hungary.
Afnan Al DoghmiDepartment of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, 6726 Szeged, Hungary.ORCID 0000-0003-3242-9859
János BalázsDepartment of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, 6726 Szeged, Hungary.ORCID 0000-0003-1775-6915
Zita SzalaiDepartment of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, 6726 Szeged, Hungary.
Ágnes FerenczDepartment of Biochemistry and Molecular Biology, Faculty of Science and Informatics, University of Szeged, 6726 Szeged, Hungary.
Edit HermeszDepartment of Biochemistry and Molecular Biology, Faculty of Science and Informatics, University of Szeged, 6726 Szeged, Hungary.ORCID 0000-0002-0543-6693
Mária BagyánszkiDepartment of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, 6726 Szeged, Hungary.ORCID 0000-0003-3533-9461
Nikolett BódiDepartment of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, 6726 Szeged, Hungary.

Funding

Hungarian Academy of Sciences János Bolyai Research Scholarship (N.B.)Hungarian NKFIH fund project No. FK131789 (N.B.)New National Excellence Program of the Ministry for Culture and Innovation from the source of the National Research, Development and Innovation Fund ÚNKP-22-3-SZTE-389 (B.P.B.)New National Excellence Program of the Ministry for Culture and Innovation from the source of the National Research, Development and Innovation Fund ÚNKP-23-3-SZTE-426 (B.P.B.)
6 · The paper itself

Abstract

BACKGROUND/

objectivesType 1 diabetes affects cytokines as potential inducers of NFκB signalling involved in inflammation and neuronal survival. Our goal was to assess the expression of NFκB p65 and its negative regulator, Nrf2, in myenteric neurons and adjacent smooth muscle of different gut segments after chronic hyperglycaemia and immediate insulin treatment.

methodsAfter ten weeks of hyperglycaemia, intestinal samples of control, streptozotocin-induced diabetic and insulin-treated diabetic rats were prepared for fluorescent immunohistochemistry, immunogold electron microscopy, ELISA and qPCR.

resultsIn the diabetic rats, the proportion of NFκB p65-immunoreactive myenteric neurons decreased significantly in the duodenum and increased in the ileum. The density of NFκB p65-labelling gold particles increased in the ileal but remained unchanged in the duodenal ganglia. Meanwhile, both total and nuclear Nrf2 density increased in the myenteric neurons of the diabetic duodenum. In smooth muscle, NFκB p65 and Nrf2 density increased in the small intestine of diabetic rats. While on the mRNA level, NFκB p65 and Nrf2 were induced, on the protein level, NFκB p65 increased and Nrf2 decreased in muscle/myenteric plexus homogenates. Insulin treatment had protective effects.

conclusionsOur findings reveal a segment-specific NFκB and Nrf expression in myenteric neurons and ganglionic muscular environments, which may contribute to regional neuronal survival and motility disturbances in diabetes.

Indexed as

animal modelenteric neuronsgut segmentshyperglycaemiainsulinintestinal smooth musclemyenteric plexusNFκBNrf2type 1 diabetes

Identifiers

PMID39457659
PMCPMC11504535

What Socratic 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 Socratic graph.