Evidence map›Paper›PMID 36738240›Full record

ArticleRedox report : communications in free radical research2023

Dexmedetomidine postconditioning attenuates myocardial ischemia/reperfusion injury by activating the Nrf2/Sirt3/SOD2 signaling pathway in the rats.

Bin Hu, Tian Tian, Xin-Tao Li, Pei-Pei Hao, Wei-Chao Liu, Ying-Gui Chen, Tian-Yu Jiang, Pei-Shan Chen, Yi Cheng, Fu-Shan Xue

Open access · goldAbstract read
In one paragraph

Article in Redox report : communications in free radical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

25 citing papers in PubMed, 33 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

10 authors at 1 institution in 1 country.

Bin HuDepartment of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.ORCID 0000-0002-7380-0151
Tian TianDepartment of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.ORCID 0000-0003-4180-3013
Xin-Tao LiDepartment of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.ORCID 0000-0003-3419-2357
Pei-Pei HaoDepartment of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.ORCID 0000-0003-0969-4910
Wei-Chao LiuDepartment of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.ORCID 0000-0002-5458-8749
Ying-Gui ChenDepartment of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.ORCID 0000-0002-5858-1560
Tian-Yu JiangDepartment of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.ORCID 0000-0002-6465-7701
Pei-Shan ChenDepartment of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.ORCID 0000-0002-5056-1725
Yi ChengDepartment of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.ORCID 0000-0001-8934-726X
Fu-Shan XueDepartment of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.ORCID 0000-0002-1028-6036
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo observe the protective effects of dexmedetomidine (Dex) postconditioning on myocardial ischemia/reperfusion injury (IRI) and to explore its potential molecular mechanisms.

methodsOne-hundred forty-seven male Sprague-Dawley rats were randomly divided into five groups receiving the different treatments: Sham, ischemia/reperfusion (I/R), Dex, Brusatol, Dex + Brusatol. By the

resultsDex postconditioning significantly alleviated myocardial IRI, decreased intracellular ROS and myocardial tissue MDA level, increased SOD and GSH-PX activities. Dex postconditioning significantly up-regulated myocardial expression of Bcl-2, down-regulated Bax and cleaved caspase-3 and decreased cardiomyocyte apoptosis rate. furthermores, Dex postconditioning promoted Nrf2 nuclear translocation, increased myocardial expression of Sirt3 and SOD2 and decreased Ac-SOD2. However, brusatol reversed cardioprotective benefits of Dex postconditioning, significantly decreased Dex-induced Nrf2 nuclear translocation and reduced myocardial expression of Sirt3 and SOD2.

conclusionsDex postconditioning can alleviate myocardial IRI by suppressing oxidative stress and apoptosis, and these beneficial effects are at least partly mediated by activating the Nrf2/Sirt3/SOD2 signaling pathway.

Indexed as

DexmedetomidineMyocardial Reperfusion InjuryReperfusion InjurySirtuin 3AnimalsApoptosisMaleNF-E2-Related Factor 2QuassinsRatsRats, Sprague-DawleyReactive Oxygen SpeciesSignal TransductionSirtuinsSuperoxide DismutaseSuperoxide Dismutase 2brusatolDexmedetomidineNfe2l2 protein, ratNF-E2-Related Factor 2QuassinsReactive Oxygen SpeciesSIRT3 protein, ratSirtuin 3SirtuinsSuperoxide DismutaseSuperoxide Dismutase 2apoptosisDexmedetomidinemyocardial ischemia/reperfusion injuryNrf2/Sirt3/SOD2 signaling pathwayoxidative stress

Identifiers

PMID36738240
PMCPMC9904316
OpenAlexW4319216220

What Socratic holds

Textmetadata
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.