Evidence map›Paper›PMID 29033541›Full record

ArticleDrug design, development and therapy2017

Dexmedetomidine reduces the neuronal apoptosis related to cardiopulmonary bypass by inhibiting activation of the JAK2-STAT3 pathway.

Yanhua Chen, Xu Zhang, Bingdong Zhang, Guodong He, Lifang Zhou, Yubo Xie

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

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  12. Dexmedetomidine pretreatment alleviates cerebral ischemia/reperfusion injury by inhibiting neuroinflammation through the JAK2/STAT3 pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022
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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 3 institutions in 2 countries.

Yanhua Chen *Department of Anesthesiology, Cardiovascular Institute.
Xu Zhang *Department of Anesthesiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Bingdong ZhangDepartment of Anesthesiology, Cardiovascular Institute.
Guodong HeDepartment of Anesthesiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Lifang ZhouDepartment of Anesthesiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Yubo XieDepartment of Anesthesiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
First Affiliated Hospital of GuangXi Medical University · CNCardiovascular Institute Hospital · JPGuangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiopulmonary bypass (CPB) constitutes one of the primary methodologies pertaining to cardiac surgery. However, this form of surgery can cause damage to the body. Many studies have reported that dexmedetomidine confers cerebral protection. In this study, we aimed to investigate the effect and mechanism of dexmedetomidine on neuronal apoptosis caused by CPB. Here, rats were treated with different doses of dexmedetomidine by intravenous infusion 2 hours after CPB. We observed that dexmedetomidine treatment to rats reduces the S100β, NSE levels in plasma, and neuronal apoptosis following CPB in a dose-dependent manner. Furthermore, we observed that the beneficial effect of dexmedetomidine treatment following CPB was associated with a reduction in IL6, an inflammatory cytokine in plasma and cortex. Our results suggest that dexmedetomidine provides neuroprotective effects by inhibiting inflammation and reducing neuronal apoptosis. There was a correlation between the protective effect on the brain and the dose of dexmedetomidine. In addition, dexmedetomidine administration inhibits phosphorylation of JAK2 and STAT3 proteins in the hippocampus of rats 2 hours after CPB. Therefore, we speculate that the JAK2-STAT3 pathway plays an important role in the neuroprotective effects of dexmedetomidine following brain injury induced by CPB.

Indexed as

AnimalsApoptosisBrainCardiopulmonary BypassCaspase 3DexmedetomidineInterleukin-6Janus Kinase 2MaleNeuroprotective AgentsPhosphopyruvate HydratasePhosphorylationRatsRats, Sprague-DawleySignal TransductionSTAT3 Transcription FactorCaspase 3DexmedetomidineInterleukin-6Jak2 protein, ratJanus Kinase 2Neuroprotective AgentsPhosphopyruvate HydrataseStat3 protein, ratSTAT3 Transcription Factorapoptosiscardiopulmonary bypassdexmedetomidineJAK2neuroprotective effectSTAT3

Identifiers

PMID29033541
PMCPMC5628699
OpenAlexW2756718435

What OpenQuestion 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 OpenQuestion graph.