Evidence map›Paper›PMID 24058562›Full record

ArticlePloS one2013

Hydrogen sulfide preconditioning protects rat liver against ischemia/reperfusion injury by activating Akt-GSK-3β signaling and inhibiting mitochondrial permeability transition.

Qingqing Zhang, Hailong Fu, Hao Zhang, Fengying Xu, Zui Zou, Meng Liu, Quanxing Wang, Mingyong Miao, Xueyin Shi

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

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
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  8. Sulfide quinone oxidoreductase contributes to voltage sensing of the mitochondrial permeability transition pore.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  9. Article
  10. Review
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  15. Article
  16. Review
  17. Article
  18. Hydrogen sulfide inhibits CaAmerican journal of physiology. Endocrinology and metabolism · 2019
    Article
  19. Hepatoprotective effect of sodium hydrosulfide on hepatic encephalopathy in rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019
    Article
  20. Review
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

9 authors at 1 institution in 1 country.

Qingqing ZhangDepartment of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Hailong Fu
Hao Zhang
Fengying Xu
Zui Zou
Meng Liu
Quanxing Wang
Mingyong Miao
Xueyin Shi
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hydrogen sulfide (H2S) is the third most common endogenously produced gaseous signaling molecule, but its impact on hepatic ischemia/reperfusion (I/R) injury, especially on mitochondrial function, remains unclear. In this study, rats were randomized into Sham, I/R, ischemia preconditioning (IPC) or sodium hydrosulfide (NaHS, an H2S donor) preconditioning groups. To establish a model of segmental (70%) warm hepatic ischemia, the hepatic artery, left portal vein and median liver lobes were occluded for 60 min and then unclamped to allow reperfusion. Preconditioning with 12.5, 25 or 50 μmol/kg NaHS prior to the I/R insult significantly increased serum H2S levels, and, similar to IPC, NaHS preconditioning decreased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in the plasma and prevented hepatocytes from undergoing I/R-induced necrosis. Moreover, a sub-toxic dose of NaHS (25 μmol/kg) did not disrupt the systemic hemodynamics but dramatically inhibited mitochondrial permeability transition pore (MPTP) opening and thus prevented mitochondrial-related cell death and apoptosis. Mechanistic studies revealed that NaHS preconditioning markedly increased the expression of phosphorylated protein kinase B (p-Akt), phosphorylated glycogen synthase kinase-3 beta (p-GSK-3β) and B-cell lymphoma-2 (Bcl-2) and decreased the release of mitochondrial cytochrome c and cleaved caspase-3/9 levels. Therefore, NaHS administration prior to hepatic I/R ameliorates mitochondrial and hepatocellular damage through the inhibition of MPTP opening and the activation of Akt-GSK-3β signaling. Furthermore, this study provides experimental evidence for the clinical use of H2S to reduce liver damage after perioperative I/R injury.

Indexed as

Ischemic PreconditioningAnimalsApoptosisAspartate AminotransferasesCalciumCaspase 3Caspase 9Cytochromes cEnzyme ActivationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHemodynamicsHydrogen SulfideLiverMaleMitochondrial Membrane Transport ProteinsAspartate AminotransferasesCalciumCaspase 3Caspase 9Cytochromes cGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratHydrogen SulfideMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreProtective AgentsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2

Identifiers

PMID24058562
PMCPMC3772845
OpenAlexW2001320749

What OpenQuestion 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 OpenQuestion graph.