Evidence map›Paper›PMID 38376046›Full record

ArticleBrain and behavior2024

Nicorandil attenuates cognitive impairment after traumatic brain injury via inhibiting oxidative stress and inflammation: Involvement of BDNF and NGF.

Yaoyan Tu, Desen Han, Yanjun Liu, Dequan Hong, Rehua Chen

Open access · goldAbstract read
In one paragraph

Article in Brain and behavior, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 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

5 authors at 1 institution in 1 country.

Yaoyan TuDepartment of Emergency and Trauma Center, Nanchang First Hospital, Nanchang, Jiangxi, China.
Desen HanDepartment of Emergency and Trauma Center, Nanchang First Hospital, Nanchang, Jiangxi, China.
Yanjun LiuDepartment of Emergency and Trauma Center, Nanchang First Hospital, Nanchang, Jiangxi, China.
Dequan HongDepartment of Emergency and Trauma Center, Nanchang First Hospital, Nanchang, Jiangxi, China.
Rehua ChenDepartment of Emergency and Trauma Center, Nanchang First Hospital, Nanchang, Jiangxi, China.ORCID 0009-0001-4001-4437
Nanchang University · CN

Funding

Nanchang Science and Technology Support Plan Project 2022-KJZC-001
6 · The paper itself

Abstract

background and purposeCognitive impairment is a prevalent adverse consequence of traumatic brain injury (TBI). The neuroprotective effects of nicorandil (N-(2-hydroxyethyl)-nicotinamide nitrate) has been previously documented, yet its protective effects against cognitive dysfunction post-TBI remain unclear. Hence, the present study was aimed to evaluate whether nicorandil attenuates cognitive dysfunction in TBI rats and the underlying mechanism behind this process.

methodsThe TBI model was established with a controlled cortical impact (CCI). The effects of nicorandil on cognitive dysfunction of rats with TBI were examined through Novel object recognition (NOR) test, Y-maze test, and Morris water maze (MWM) task. After behavioral tests, hippocampal tissue was collected for Quantitative real-time PCR, Western blot analysis, and Enzyme-linked immunosorbent assay (ELISA) assay.

resultsWe observed that nicorandil administration effectively ameliorates learning and memory impairment in TBI rats. Alongside, nicorandil treatment attenuated oxidative stress in the hippocampus of TBI rats, characterized by the decreased reactive oxygen species generation, malondialdehyde, and protein carbonyls levels, and concurrent promotion of antioxidant-related factors (including superoxide dismutase, glutathione peroxidase, and catalase) activities. Additionally, nicorandil treatment attenuated the inflammatory response in the hippocampus of TBI rat, as evidenced by the upregulated levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α), as well as the downregulated level of IL-10. Mechanistically, nicorandil treatment significantly enhanced the mRNA and protein levels of neurotrophic factors, brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the hippocampus of TBI rats.

conclusionThese findings suggest that nicorandil mitigates cognitive impairment after TBI by suppressing oxidative stress and inflammation, potentially through enhancing BDNF and NGF levels.

Indexed as

Brain Injuries, TraumaticCognitive DysfunctionNicorandilAnimalsBrain-Derived Neurotrophic FactorDisease Models, AnimalHippocampusInflammationMaze LearningNerve Growth FactorOxidative StressRatsBrain-Derived Neurotrophic FactorNerve Growth FactorNicorandilcognitive impairmentneurotrophic factornicorandiltraumatic brain injury

Identifiers

PMID38376046
PMCPMC10757892
OpenAlexW4390474397

What Socratic holds

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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.