ArticleFrontiers in molecular neuroscience2022
Necrosulfonamide Alleviates Acute Brain Injury of Intracerebral Hemorrhage
Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Non-apoptotic Regulated Cell Death Mechanisms in Sepsis and their Therapeutic Potential.Inflammation · 2026Review
- MLKL Modulates Necroptosis and Neuroinflammation in a Mouse Model of MS.Inflammation · 2025Article
- Pseudorabies virus induces natural killer cell depletion by GSDMD-mediated inflammation and pyroptosis to promote infection and lung injury.Journal of virology · 2025Article
- Sulphonylureas as Adjunct Therapeutic Agents in the Treatment of Autoimmune Conditions: A Narrative Review.Pharmacology research & perspectives · 2025Review
- MLKL Inhibitor Reduces Oxidative Stress, Inflammation, and Dopaminergic Neuronal Cell Death in MPTP-Induced Parkinson's Disease Mouse Model.Biomolecules & therapeutics · 2025Article
- Neuroprotective role of morin hydrate on 3-nitropropionic acid-elicited huntington's disease: in vivo investigation of RIPK1/RIPK3/MLKL necroptosis signaling pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- NLRP3 inflammasome in neuroinflammation and central nervous system diseases.Cellular & molecular immunology · 2025Review
- Spermidine Exerts Neuroprotective Effects Following Intracerebral Hemorrhage in Mice Through Anti-Inflammation and Blood-Brain Barrier Protection.Journal of inflammation research · 2025Article
- GSDMD/Drp1 signaling pathway mediates hippocampal synaptic damage and neural oscillation abnormalities in a mouse model of sepsis-associated encephalopathy.Journal of neuroinflammation · 2024Article
- Ion Channel Dysregulation Following Intracerebral Hemorrhage.Neuroscience bulletin · 2024Review
- Necroptosis inhibitors: mechanisms of action and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2024Review
- Necrostatin-1: a promising compound for neurological disorders.Frontiers in cellular neuroscience · 2024Review
- Therapeutic potential of PANoptosis: innate sensors, inflammasomes, and RIPKs in PANoptosomes.Trends in molecular medicine · 2024Review
- Assessing the cardioprotective effect of necrosulfonamide in doxorubicin-induced cardiotoxicity in mice.Journal of medicine and life · 2023Article
- Omarigliptin inhibits brain cell ferroptosis after intracerebral hemorrhage.Scientific reports · 2023Article
- Necrosulfonamide exerts neuroprotective effect by inhibiting necroptosis, neuroinflammation, and α-synuclein oligomerization in a subacute MPTP mouse model of Parkinson's disease.Scientific reports · 2023Article
- The regulation of self-tolerance and the role of inflammasome molecules.Frontiers in immunology · 2023Review
- Breaking bad: necroptosis in the pathogenesis of gastrointestinal diseases.Frontiers in immunology · 2023Review
- Approaches to Evaluating Necroptosis in Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Intracerebral hemorrhage (ICH) is the most lethal subtype of stroke, without effective treatment. Necrosulfonamide (NSA), a specific inhibitor for mixed lineage kinase domain-like protein, has been reported to exert neuroprotective effects in neurological diseases by ameliorating neuroinflammation and necroptosis. We hypothesized that NSA would alleviate acute brain injury and improve behavioral outcomes after ICH. Materials and Methods: Male adult C57BL/6 mice were assigned randomly into three groups. In vehicle and treatment groups, animals were injected with collagenase VII to induce ICH. The solvent (0.25% DMSO) and NSA (5 mg/kg) were administrated intraperitoneally twice a day, respectively. The sham group was injected with saline and administrated with DMSO. The brain hematoma volume, inflammatory factors, and blood-brain barrier permeability were measured on day 3 after the operation. Fluorescent double immunostaining was performed to evaluate the neuronal death. Neurological functions were assessed. Results: In the NSA group, the hematoma size was significantly reduced, inflammatory cells and cytokines were suppressed, and the blood-brain barrier was protected compared to vehicle controls. NSA dramatically reduced the death of neurons and improved the performance of neurological functions after ICH. Conclusion: Necrosulfonamide has a neuroprotective role in alleviating acute brain injury in a mouse ICH model, and this is associated with reduced neuroinflammation and necroptosis.
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