Evidence map›Paper›PMID 36358571›Full record

ArticleAntioxidants (Basel, Switzerland)2022

Dexmedetomidine Attenuates Apoptosis and Neurological Deficits by Modulating Neuronal NADPH Oxidase 2-Derived Oxidative Stress in Neonates Following Hypoxic Brain Injury.

Xiaohui Chen, Dongtai Chen, Pinzhong Chen, Andi Chen, Jianhui Deng, Jianjie Wei, Weian Zeng, Xiaochun Zheng

Abstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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.

Xiaohui ChenDepartment of Anesthesiology, Shengli Clinical Medical College, Fujian Medical University, Fujian Provincial Hospital, Fuzhou 350001, China.ORCID 0000-0002-1864-6729
Dongtai ChenDepartment of Anesthesiology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangzhou 510060, China.ORCID 0000-0003-0193-2902
Pinzhong ChenDepartment of Anesthesiology, Shengli Clinical Medical College, Fujian Medical University, Fujian Provincial Hospital, Fuzhou 350001, China.
Andi ChenDepartment of Anesthesiology, Shengli Clinical Medical College, Fujian Medical University, Fujian Provincial Hospital, Fuzhou 350001, China.
Jianhui DengDepartment of Anesthesiology, Shengli Clinical Medical College, Fujian Medical University, Fujian Provincial Hospital, Fuzhou 350001, China.
Jianjie WeiDepartment of Anesthesiology, Shengli Clinical Medical College, Fujian Medical University, Fujian Provincial Hospital, Fuzhou 350001, China.
Weian ZengDepartment of Anesthesiology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangzhou 510060, China.
Xiaochun ZhengDepartment of Anesthesiology, Shengli Clinical Medical College, Fujian Medical University, Fujian Provincial Hospital, Fuzhou 350001, China.ORCID 0000-0002-6213-0789

Funding

National Natural Science Foundation of China Grant Nos. 82001166 and and 82171186Natural Science Foundation of Fujian Province Grant No. 2020J05261the Joint Funds for the Innovation of Science and Technology, Fujian Province Grant Nos. 2019Y9028 and 2019Y9023the Training Project for Talents of Fujian Provincial Health Commission Grant No. 2020GGA013
6 · The paper itself

Abstract

Hypoxic-ischemic brain injury is an important cause of neonatal neurological deficits. Our previous study demonstrated that dexmedetomidine (Dex) provided neuroprotection against neonatal hypoxic brain injury; however, the underlying mechanisms remain incompletely elucidated. Overactivation of NADPH oxidase 2 (NOX2) can cause neuronal apoptosis and neurological deficits. Hence, we aimed to investigate the role of neuronal NOX2 in Dex-mediated neuroprotection and to explore its potential mechanisms. Hypoxic injury was modeled in neonatal rodents in vivo and in cultured hippocampal neurons in vitro. Our results showed that pre- or post-treatment with Dex improved the neurological deficits and alleviated the hippocampal neuronal damage and apoptosis caused by neonatal hypoxia. In addition, Dex treatment significantly suppressed hypoxia-induced neuronal NOX2 activation; it also reduced oxidative stress, as evidenced by decreases in intracellular reactive oxygen species (ROS) production, malondialdehyde, and 8-hydroxy-2-deoxyguanosine, as well as increases in the antioxidant enzymatic activity of superoxide dismutase and glutathione peroxidase in neonatal rat hippocampi and in hippocampal neurons. Lastly, the posthypoxicneuroprotective action of Dex was almost completely abolished in NOX2-deficient neonatal mice and NOX2-knockdown neurons. In conclusion, our data demonstrated that neuronal NOX2-mediated oxidative stress is involved in the neuroprotection that Dex provides against apoptosis and neurological deficits in neonates following hypoxia.

Indexed as

dexmedetomidinehypoxic brain injuryNADPH oxidase 2neonatesneurological deficitsneuronal apoptosisoxidative stress

Identifiers

PMID36358571
PMCPMC9686745

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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.