Evidence map›Paper›PMID 27069541›Full record

ArticleAmerican journal of translational research2016

Dexmedetomidine alleviates postoperative cognitive dysfunction by inhibiting neuron excitation in aged rats.

Bo Xiong, Qiqing Shi, Hao Fang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

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  11. A Review of the Biological Mechanisms of Dexmedetomidine for Postoperative Neurocognitive Disorders.Medical science monitor : international medical journal of experimental and clinical research · 2022
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  17. Different Anesthetic Drugs Mediate Changes in Neuroplasticity During Cognitive Impairment in Sleep-Deprived Rats via Different Factors.Medical science monitor : international medical journal of experimental and clinical research · 2021
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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

3 authors at 3 institutions in 1 country.

Bo XiongDepartment of Anesthesiology, Fudan University Shanghai Cancer Center Shanghai, China.
Qiqing ShiDepartment of Anesthesiology, Children's Hospital of Fudan University Shanghai, China.
Hao FangDepartment of Anesthesiology, Jinshan Hospital Fudan UniversityShanghai, China; Department of Anesthesiology, Zhongshan Hospital Fudan UniversityShanghai, China.
Children's Hospital of Fudan University · CNFudan University Shanghai Cancer Center · CNJinshan Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The perioperative stress response is one of the factors leading to postoperative cognitive dysfunction (POCD). Dexmedetomidine (Dex) can reduce the stress response and hippocampus neuroapoptosis, but its mechanism of action on POCD remains unknown. This study investigated the protective effect and possible mechanism of Dex on POCD in aged rats. Ninety-six aged male rats were randomly divided into four groups (n = 24 rats per group): a non-surgical control group, a surgical (model) group, a surgical group receiving a high dose of Dex (12 μg/kg), and a surgical group receiving a low dose of Dex (3 μg/kg). Cognitive function and neuronal apoptosis were evaluated after splenectomy. Compared with the control group, the model group had significantly longer escape latencies and fewer platform crossings in the Morris water-maze test. Immunohistochemistry showed that relaxin-3 and c-fos positive neurons in the hippocampus increased on postoperative days 1 and 3. Greater downregulation of the Bcl-2 protein and upregulation of Fas, caspase-8, and caspase-9 significantly increased neuroapoptosis in the model group. Compared with the model group, rats given Dex had (1) shorter escape latencies, (2) more platform crossings, (3) fewer relaxin-3 and c-fos positive neurons in the hippocampal CA1 area, (4) upregulation of Bcl-2, (5) downregulation of Fas, caspase-8, and caspase-9 proteins, and (6) decreased neuroapoptosis in the hippocampus. Thus, our data suggest that Dex may improve cognitive functioning in aged rats by inhibiting neural over-excitability. The mechanism may operate by restraining relaxin-3 and c-fos expression.

Indexed as

agingDexmedetomidine (Dex)hippocampusneuroapoptosispostoperative cognitive dysfunctionrats

Identifiers

PMID27069541
PMCPMC4759417
OpenAlexW2341728189

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.