ArticleInternational journal of molecular medicine2018
Neuroprotective effects of hydrogen sulfide on sodium azide-induced oxidative stress in PC12 cells.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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.
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.
Who cites it
21 citing papers in PubMed, 46 citations in OpenAlex.
- Uptake Inhibition to Improve Bioavailability of Nanoparticle-Mediated Growth Factor Delivery to the Corneal Epithelium.ACS pharmacology & translational science · 2025Article
- Exploring the Mechanism of HInternational journal of molecular sciences · 2024Article
- Post-Traumatic Expressions of Aromatase B, Glutamine Synthetase, and Cystathionine-Beta-Synthase in the Cerebellum of Juvenile Chum Salmon,International journal of molecular sciences · 2024Article
- Characterization and mechanism of simultaneous degradation of aflatoxin BFrontiers in microbiology · 2024Article
- Static Magnetic Field Reduces Intracellular ROS Levels and Protects Cells Against Peroxide-Induced Damage: Suggested Roles for Catalase.Neurotoxicity research · 2023Article
- A mitochondria-targeted chemiluminescent probe for detection of hydrogen sulfide in cancer cells, human serum andRSC chemical biology · 2023Article
- Role of 3-Mercaptopyruvate Sulfurtransferase (3-MST) in Physiology and Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Review
- Protein Delivery to Cytosol by Cell-Penetrating Peptide Bearing Tandem Repeat Penetration-Accelerating Sequence.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Hydrogen Sulfide (HCurrent neuropharmacology · 2022Review
- Bergenin ameliorates cognitive deficits and neuropathological alterations in sodium azide-induced experimental dementia.Frontiers in pharmacology · 2022Article
- PTD4 Peptide Increases Neural Viability in an In Vitro Model of Acute Ischemic Stroke.International journal of molecular sciences · 2021Article
- SIRT1 Mediates HNeurochemical research · 2021Article
- Biological Effects of Hydrogen Sulfide and Its Protective Role in Intracerebral Hemorrhage.Journal of molecular neuroscience : MN · 2020Review
- PycnogenolNutrients · 2020Article
- S-methyl-L-cysteine Protects against Antimycin A-induced Mitochondrial Dysfunction in Neural Cells via Mimicking Endogenous Methionine-centered Redox Cycle.Current medical science · 2020Article
- Biologic Effect of Hydrogen Sulfide and Its Role in Traumatic Brain Injury.Oxidative medicine and cellular longevity · 2020Review
- The effects of intravitreal HInternational journal of experimental pathology · 2019Article
- Potential for therapeutic use of hydrogen sulfide in oxidative stress-induced neurodegenerative diseases.International journal of medical sciences · 2019Review
- Nrf2 Signaling in Sodium Azide-Treated Oligodendrocytes Restores Mitochondrial Functions.Journal of molecular neuroscience : MN · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common neurodegenerative disorder, responsible for >50% of all dementia cases. Sodium azide (NaN3) inhibits cytochrome oxidase by irreversibly binding to the heme cofactor and selectively reducing the complex IV activity, which is present in post‑mortem AD brains. Previous data demonstrated that hydrogen sulfide (H2S), the third endogenous gaseous mediator, exerted protective effects against neuronal damage. Therefore, it was hypothesized that H2S may be able to scavenge excess reactive oxygen species (ROS), thereby protecting against oxidative stress and cell death. In the present study, it was observed that cell viability decreased in a concentration-dependent manner 12 h after NaN3 treatment (20, 30 and 50 mmol/l). A decrease in cell viability (to 51±3%) was observed 12 h after treatment with 30 mM NaN3. NaN3 treatment also led to decreased mitochondrial membrane potential, increased lipid peroxidation (excessive production of malondialdehyde), and increased the protein expression levels of caspase-3. Pretreatment with H2S (200 µmol/l) attenuated NaN3-mediated apoptosis, and the anti-apoptotic action of H2S was partially dependent on suppressing the production of ROS. The findings of the present study suggested that H2S exerted a neuroprotective effect against NaN3-induced neurotoxicity through mechanisms related to anti-oxidation and anti-apoptosis. Therefore, the findings of the present study suggest there may be a promising future for H2S-based preventions and therapies for neuronal damage following exposure to NaN3.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.