Evidence map›Paper›PMID 27147542›Full record

ArticleBritish journal of anaesthesia2016

Inhibiting NADPH oxidase protects against long-term memory impairment induced by neonatal sevoflurane exposure in mice.

Z Sun, M Satomoto, Y U Adachi, H Kinoshita, K Makita

Open access · bronzeAbstract readComment
In one paragraph

Article in British journal of anaesthesia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 60 citations in OpenAlex.

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  11. Controversies in anesthesia-induced developmental neurotoxicity.Best practice & research. Clinical anaesthesiology · 2023
    Review
  12. Review
  13. Neonatal Anesthesia and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022
    Review
  14. Review
  15. Article
  16. Oxidative Stress as a Common Key Event in Developmental Neurotoxicity.Oxidative medicine and cellular longevity · 2021
    Review
  17. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Z SunDepartment of Anaesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
M SatomotoDepartment of Anaesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan satomoto.mane@tmd.ac.jp.
Y U AdachiDepartment of Anaesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
H KinoshitaDepartment of Anaesthesiology, Aichi Medical University School of Medicine, Aichi, Japan.
K MakitaDepartment of Anaesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Tokyo Medical and Dental University · JPAichi Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeonatal exposure to anaesthetics such as sevoflurane has been reported to result in behavioural deficits in rodents. However, while oxidative injury is thought to play an underlying pathological role, the mechanisms of neurotoxicity remain unclear. In the present study, we investigated whether the NADPH oxidase inhibitor apocynin protects against long-term memory impairment produced by neonatal sevoflurane exposure in mice.

methodsPostnatal day six mice were divided into four groups; (1) non-anaesthesia, (2) intraperitoneal apocynin (50 mg kg(-1)) treatment, (3) 3% sevoflurane exposure for 6 h, and (4) apocynin treatment combined with sevoflurane exposure. Superoxide concentrations and NADPH oxidase expression in the brain were determined using dihydroethidium fluorescence and immunoblotting, respectively. Cleaved caspase-3 immunoblotting was used for the detection of apoptosis, and cytochrome c immunoblotting was performed to evaluate mitochondrial function. Long-term cognitive impairment was evaluated using the fear conditioning test in adulthood.

resultsSevoflurane exposure increased concentrations of superoxide (109%) and the NADPH oxidase subunit p22phox (39%) in the brain, and apocynin abolished these increases. Neonatal sevoflurane exposure caused learning deficits in adulthood. Apocynin also maintained long-term memory function in mice given neonatal sevoflurane exposure, and it reduced apoptosis and decreased cytochrome c concentrations in the brains of these mice.

conclusionsApocynin reduces neuronal apoptosis and protects against long-term memory impairment in mice, neonatally exposed to sevoflurane by reducing superoxide concentrations. These findings suggest that NADPH oxidase inhibitors may protect against cognitive dysfunction resulting from neonatal anaesthesia.

Indexed as

Animals, NewbornNADPH OxidasesAnimalsMemory, Long-TermMethyl EthersMiceMice, Inbred C57BLSevofluraneMethyl EthersNADPH OxidasesSevofluraneanaesthesiaanaestheticsbrainneurotoxicitypaediatricsevoflurane

Identifiers

PMID27147542
PMCPMC4913390
OpenAlexW2346322586

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.