Evidence map›Paper›PMID 31028241›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2019

Effects of Sevoflurane Pretreatment on Myocardial Ischemia-Reperfusion Injury Through the Akt/Hypoxia-Inducible Factor 1-alpha (HIF-1α)/Vascular Endothelial Growth Factor (VEGF) Signaling Pathway.

Jingwei Dong, Mingjun Xu, Wenyu Zhang, Xiangming Che

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 31 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

4 authors at 2 institutions in 1 country.

Jingwei DongDepartment of Anesthesiology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, China (mainland).
Mingjun XuDepartment of Anesthesiology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, China (mainland).
Wenyu ZhangDepartment of Anesthesiology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, China (mainland).
Xiangming CheDepartment of Anesthesiology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, China (mainland).
Beijing Obstetrics and Gynecology Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND The aim of this study was to investigate the effects of sevoflurane (SEV) on myocardial ischemia/reperfusion (I/R) injury in rats and its mechanism. MATERIAL AND METHODS Sixty male Sprague-Dawley rats were randomly divided into 3 groups: Sham group (n=20), I/R group (n=20) and I/R+SEV group (n=20). The I/R model was established by ligating and recanalizing the left anterior descending coronary artery (LAD). Triphenyl tetrazolium chloride (TTC) test and echocardiography (ECG) were used for analysis. Hematoxylin and eosin (H&E) staining was applied to detect the morphological changes. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was conducted to detect the apoptosis levels. The expression level of superoxide dismutase 2 (SOD2) was measured. Finally, the effect of SEV on the protein kinase B (Akt)/hypoxia-inducible factor 1-alpha (HIF-1alpha)/vascular endothelial growth factor (VEGF) signaling pathway was detected via western blotting. RESULTS SEV could significantly improve I/R-induced cardiac insufficiency, inhibit cardiac infarction, and as well as reduce the infarction area from 53.21±2.11% to 32.33±3.49% (P<0.05). Compared with rats in I/R group, the cardiac myofilament was better in alignment, degradation and necrosis were milder, and cell edema was notably reduced in the I/R+SEV group. Thus, SEV could significantly reverse the decreased expression of SOD2 caused by I/R and reduce oxidative stress in the heart (P<0.05). According to the western blotting results, SEV was capable of obviously activating the expressions of phosphorylated-Akt (p-Akt), HIF-1alpha, and VEGF. CONCLUSIONS SEV can significantly improve myocardial injury caused by I/R in rats, and its mechanism might be related to the activation of the Akt/HIF-1alpha/VEGF signaling pathway.

Indexed as

AnimalsApoptosisHypoxia-Inducible Factor 1, alpha SubunitMaleMyocardial IschemiaMyocardial ReperfusionMyocardial Reperfusion InjuryProto-Oncogene Proteins c-aktRandom AllocationRatsRats, Sprague-DawleySevofluraneSignal TransductionVascular Endothelial Growth Factor AHypoxia-Inducible Factor 1, alpha SubunitProto-Oncogene Proteins c-aktSevofluraneVascular Endothelial Growth Factor Avascular endothelial growth factor A, rat

Identifiers

PMID31028241
PMCPMC6501450
OpenAlexW2941614495

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.