Evidence map›Paper›PMID 28937042›Full record

ArticleChinese medical journal2017

Sirtuin 1 Mediates Hydrogen Sulfide-induced Cytoprotection Effects in Neonatal Mouse Cardiomyocytes.

Ai-Jun Liu, Bin Li, Ming Yang, Yang Liu, Ying-Long Liu, Jun-Wu Su

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

Article in Chinese medical journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 15 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

6 authors at 2 institutions in 1 country.

Ai-Jun LiuDepartment of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Bin LiDepartment of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Ming YangDepartment of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Yang LiuDepartment of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Ying-Long LiuDepartment of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Jun-Wu SuDepartment of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Capital Medical University · CNBeijing Anzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCurrent knowledge indicates that oxidative damage and the following inflammation is pivotal pathway for myocardial cell death. In recent decades, hydrogen sulfide (H2S) has been identified as a novel endogenous vasodilator and neuromodulator due to its antioxidation capacity. However, whether H2S pretreatment in neonatal mouse cardiomyocytes is a protection effect against oxidative stress remains elusive.

methodsPrimary neonatal mouse cardiomyocytes were isolated and cultured, subsequently, pretreated with the H2S donor, sodium hydrosulfide (NaHS). Cell viability, lactate dehydrogenase (LDH) release, and reactive oxygen species (ROS) production are evaluated. The levels of superoxide dismutase (Sod2) and Sirtuin 1 (Sirt1), a deacetylation enzyme, were detected by Western blotting. The statistics was performed using independent-sample t-test.

resultsNaHS (100 μmol/L) had no toxicity to primary neonatal mouse cardiomyocytes. Furthermore, NaHS pretreatment significantly improved neonatal mouse cardiomyocytes survival after H2O2-induced cell death, indicated by the decrease in LDH release (40.00 ± 2.65% vs. 65.33 ± 4.33%, P < 0.01) and ROS production (1.90 ± 0.33 vs. 4.56 ± 0.56, P < 0.05), and that the salubrious effect was accompanied by the upregulation of Sod2 expression. In addition, the study showed that NaHS pretreatment improved mitochondrial DNA number in neonatal mouse cardiomyocyte. Furthermore, the result demonstrated NaHS increased the expression of Sirt1 in neonatal mouse cardiomyocyte. Ex 527, an inhibitor of Sirt1, could attenuate these effects of NaHS-induced Sod2 expression and mtDNA number increase, furthermore, abrogate the cytoprotective effects of NaHS for neonatal mouse cardiomyocytes.

conclusionSirt1 mediated H2S-induced cytoprotection effects in neonatal mouse cardiomyocytes.

Indexed as

AnimalsBlotting, WesternCells, CulturedCell SurvivalDNA Copy Number VariationsHydrogen SulfideL-Lactate DehydrogenaseMiceMyocytes, CardiacOxidative StressReactive Oxygen SpeciesSirtuin 1SulfidesHydrogen SulfideL-Lactate DehydrogenaseReactive Oxygen SpeciesSirtuin 1sodium bisulfideSulfides

Identifiers

PMID28937042
PMCPMC5634087
OpenAlexW2982962735

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.