ArticleMolecular medicine reports2017
Neuroprotective effects of hydrogen sulfide on sodium azide‑induced autophagic cell death in PC12 cells.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- Disrupted brain mitochondrial morphology after in vivo hydrogen sulfide exposure.Scientific reports · 2023Article
- Differential effects of subchronic acrylonitrile exposure on hydrogen sulfide levels in rat blood, brain, and liver.Toxicology research · 2022Article
- Zinc oxide nanoparticles effectively regulate autophagic cell death by activating autophagosome formation and interfering with their maturation.Particle and fibre toxicology · 2020Article
- Role of the protease-activated receptor 1 in regulating the function of glial cells within central and peripheral nervous system.Journal of neural transmission (Vienna, Austria : 1996) · 2019Review
- Optimization of Degradation Conditions with PRG, a Polysaccharide fromMolecules (Basel, Switzerland) · 2019Article
- Topical Administration of a Soluble TNF Inhibitor Reduces Infarct Volume After Focal Cerebral Ischemia in Mice.Frontiers in neuroscience · 2019Article
- Neuroprotective effects of hydrogen sulfide on sodium azide-induced oxidative stress in PC12 cells.International journal of molecular medicine · 2018Article
- Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors.Frontiers in molecular neuroscience · 2018Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sodium azide (NaN3) is a chemical of rapidly growing commercial importance. It is very acutely toxic and inhibits cytochrome oxidase (COX) by binding irreversibly to the heme cofactor. A previous study from our group demonstrated that hydrogen sulfide (H2S), the third endogenous gaseous mediator identified, had protective effects against neuronal damage induced by traumatic brain injury (TBI). It is well‑known that TBI can reduce the activity of COX and have detrimental effects on the central nervous system metabolism. Therefore, in the present study, it was hypothesized that H2S may provide neuroprotection against NaN3 toxicity. The current results revealed that NaN3 treatment induced non‑apoptotic cell death, namely autophagic cell death, in PC12 cells. Expression of the endogenous H2S‑producing enzymes, cystathionine‑β‑synthase and 3‑mercaptopyruvate sulfurtransferase, decreased in a dose‑dependent manner following NaN3 treatment. Pretreatment with H2S markedly attenuated the NaN3‑induced cell viability loss and autophagic cell death in a dose‑dependent manner. The present study suggests that H2S‑based strategies may have future potential in the prevention and/or therapy of neuronal damage following NaN3 exposure.
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