Evidence map›Paper›PMID 27160344›Full record

ArticleCNS neuroscience & therapeutics2016

Sodium Sulfide, a Hydrogen Sulfide-Releasing Molecule, Attenuates Acute Cerebral Ischemia in Rats.

Hao-Qiang Shi, Ying Zhang, Ming-He Cheng, Bo-Shi Fan, Jia-Sheng Tian, Jian-Guang Yu, Bing Chen

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. HAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  2. Review
  3. Role of hydrogen sulfide in subarachnoid hemorrhage.CNS neuroscience & therapeutics · 2022
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Regulation of Aqueous Humor Dynamics by Hydrogen Sulfide: Potential Role in Glaucoma Pharmacotherapy.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics
    Review
  13. Article
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

7 authors.

Hao-Qiang ShiDepartment of Pharmacy, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Ying ZhangDepartment of Pharmacology, Second Military Medical University, Shanghai, China.
Ming-He ChengDepartment of Pharmacology, Second Military Medical University, Shanghai, China.
Bo-Shi FanDepartment of Pharmacology, Second Military Medical University, Shanghai, China.
Jia-Sheng TianDepartment of Pharmacology, Second Military Medical University, Shanghai, China.
Jian-Guang YuDepartment of Pharmacology, Second Military Medical University, Shanghai, China.
Bing ChenDepartment of Pharmacy, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsAcute cerebral ischemia may lead to ischemic stroke, which is a major cause of death and disability worldwide. Hydrogen sulfide (H2 S) functions importantly in mammalian systems. The present work was designed to study the effect of sodium sulfide, a donor of H2 S, on acute cerebral ischemia.

methodsAcute cerebral focal ischemia was produced by middle cerebral artery occlusion (MCAO) in Sprague-Dawley (SD) rats. Bilateral vertebral arteries and common carotid arteries were blocked to establish cerebral global ischemia in SD rats. Acute cerebral anoxia was produced by hypobaric anoxia in C57BL/6 mice and hypoxic anoxia in SD rats. Nimodipine and aspirin were set as positive control separately.

resultsInfarct size after MCAO was decreased by sodium sulfide. Sodium sulfide improved cerebral energy metabolism after cerebral global ischemia and prolonged survival time of animals with acute cerebral anoxia. In addition, increased cerebral blood flow and decreased cerebrovascular resistance, blood viscosity, and thrombogenesis were observed in animals treated with sodium sulfide. In cultured neurons, sodium sulfide increased cell viability and decreased cell apoptosis induced by oxygen-glucose deprivation.

conclusionSodium sulfide, a H2 S donor, presents protective effect on acute cerebral ischemia, and might be a promising therapeutic drug.

Indexed as

Acute DiseaseAnalysis of VarianceAnimalsApoptosisAspirinBlood PressureCells, CulturedCell SurvivalCerebrovascular CirculationDisease Models, AnimalDogsDose-Response Relationship, DrugElectroencephalographyFibrinolytic AgentsHeart RateInfarction, Middle Cerebral ArteryAspirinFibrinolytic AgentsNeuroprotective AgentsNimodipinesodium sulfideSulfidesAcute cerebral ischemiaHydrogen sulfideSodium sulfideStroke

Identifiers

PMID27160344
PMCPMC6492871

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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.