ArticleMolecular neurobiology2016
Hydrogen Sulfide Ameliorates Early Brain Injury Following Subarachnoid Hemorrhage in Rats.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 66 citations in OpenAlex.
- Hydrogen sulfide and ferroptosis inhibition underlies the dietary restriction-induced protection against cyclophosphamide cystitis.Frontiers in pharmacology · 2025Article
- The Role of Hydrogen Sulfide in Regulation of Cell Death following Neurotrauma and Related Neurodegenerative and Psychiatric Diseases.International journal of molecular sciences · 2023Review
- Protective Effect of Hydrogen Sulfide on Cerebral Ischemia-Reperfusion Injury.Cellular and molecular neurobiology · 2023Review
- L-Cysteine attenuates osteopontin-mediated neuroinflammation following hypoxia-ischemia insult in neonatal mice by inducing S-sulfhydration of Stat3.Acta pharmacologica Sinica · 2022Article
- Role of hydrogen sulfide in subarachnoid hemorrhage.CNS neuroscience & therapeutics · 2022Review
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Differential effects of subchronic acrylonitrile exposure on hydrogen sulfide levels in rat blood, brain, and liver.Toxicology research · 2022Article
- Activation of SIRT1 Alleviates Ferroptosis in the Early Brain Injury after Subarachnoid Hemorrhage.Oxidative medicine and cellular longevity · 2022Article
- Hydrogen Sulfide Actions in the Vasculature.Comprehensive Physiology · 2021Article
- Acyl-CoA synthetase long chain family member 4 plays detrimental role in early brain injury after subarachnoid hemorrhage in rats by inducing ferroptosis.CNS neuroscience & therapeutics · 2021Article
- An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage.Frontiers in aging neuroscience · 2021Review
- L-Cysteine Provides Neuroprotection of Hypoxia-Ischemia Injury in Neonatal Mice via a PI3K/Akt-Dependent Mechanism.Drug design, development and therapy · 2021Article
- Oxidative Stress at the Crossroads of Aging, Stroke and Depression.Aging and disease · 2020Review
- Neuroinflammation Mediated by NLRP3 Inflammasome After Intracerebral Hemorrhage and Potential Therapeutic Targets.Molecular neurobiology · 2020Review
- Neuroprotective mechanism of L-cysteine after subarachnoid hemorrhage.Neural regeneration research · 2020Article
- Roles of Prokineticin 2 in Subarachnoid Hemorrhage-Induced Early Brain Injury via Regulation of Phenotype Polarization in Astrocytes.Molecular neurobiology · 2020Article
- Hydrogen Sulfide Reduces Cognitive Impairment in Rats After Subarachnoid Hemorrhage by Ameliorating Neuroinflammation Mediated by the TLR4/NF-κB Pathway in Microglia.Frontiers in cellular neuroscience · 2020Article
- CBS-Induced HEvidence-based complementary and alternative medicine : eCAM · 2020Article
- The impact of endothelial cell death in the brain and its role after stroke: A systematic review.Cell stress · 2019Review
- Tetramethylpyrazine Nitrone Reduces Oxidative Stress to Alleviate Cerebral Vasospasm in Experimental Subarachnoid Hemorrhage Models.Neuromolecular medicine · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing studies have demonstrated the neuroprotective effect of hydrogen sulfide (H2S) in central nervous system (CNS) diseases. However, the potential application value of H2S in the therapy of subarachnoid hemorrhage (SAH) is still not well known. This study was to investigate the potential effect of H2S on early brain injury (EBI) induced by SAH and explore the underlying mechanisms. The role of sodium hydrosulfide (NaHS), a donor of H2S, in SAH-induced EBI, was investigated in both in vivo and in vitro. A prechiasmatic cistern single injection model was used to produce experimental SAH in vivo. In vitro, cultured primary rat cortical neurons and human umbilical vein endothelial cells (HUVECs) were exposed to OxyHb at concentration of 10 μM to mimic SAH. Endogenous production of H2S in the brain was significantly inhibited by SAH. The protein levels of the predominant H2S-generating enzymes in the brain, including cystathionineb-synthase (CBS) and 3-mercaptopyruvate sulfur transferase (3MST), were also correspondingly reduced by SAH, while treatment with NaHS restored H2S production and the expressions of CBS and 3MST. More importantly, NaHS treatment could significantly attenuate EBI (including brain edema, blood-brain barrier disruption, brain cell apoptosis, inflammatory response, and cerebral vasospasm) after SAH. In vitro, H2S protects neurons and endothelial function by functioning as an antioxidant and antiapoptotic mediator. Our results suggest that NaSH as an exogenous H2S donor could significantly reduce EBI induced by SAH.
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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.