ArticleJournal of molecular neuroscience : MN2014
Anti-necroptosis chemical necrostatin-1 can also suppress apoptotic and autophagic pathway to exert neuroprotective effect in mice intracerebral hemorrhage model.
Article in Journal of molecular neuroscience : MN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 71 citations in OpenAlex.
- The Role of Myeloid Differentiation Factor 2 in Stroke: Mechanisms and Therapeutic Potential.Biomolecules · 2025Review
- A review of cell death pathways in hemorrhagic stroke.Frontiers in cell and developmental biology · 2025Review
- Necrostatin-1: a promising compound for neurological disorders.Frontiers in cellular neuroscience · 2024Review
- The Regulated Cell Death and Potential Interventions in Preterm Infants after Intracerebral Hemorrhage.Current neuropharmacology · 2023Review
- Necrostatin-1 decreases necroptosis and inflammatory markers after intraventricular hemorrhage in mice.Neural regeneration research · 2022Article
- Mechanistic Insight on Autophagy Modulated Molecular Pathways in Cerebral Ischemic Injury: From Preclinical to Clinical Perspective.Neurochemical research · 2022Review
- Ferroptosis-A Novel Mechanism With Multifaceted Actions on Stroke.Frontiers in neurology · 2022Review
- Ulinastatin alleviates early brain injury after intracerebral hemorrhage by inhibiting necroptosis and neuroinflammation via MAPK/NF-κB signaling pathway.Acta cirurgica brasileira · 2022Article
- Modes of Brain Cell Death Following Intracerebral Hemorrhage.Frontiers in cellular neuroscience · 2022Review
- Article
- Activated Microglia Exosomes Mediated miR-383-3p Promotes Neuronal Necroptosis Through Inhibiting ATF4 Expression in Intracerebral Hemorrhage.Neurochemical research · 2021Article
- Necrostatin-1 and necroptosis inhibition: Pathophysiology and therapeutic implications.Pharmacological research · 2021Review
- Aquaporin 4 and brain-related disorders: Insights into its apoptosis roles.EXCLI journal · 2021Review
- Emerging immune and cell death mechanisms in stroke: Saponins as therapeutic candidates.Brain, behavior, & immunity - health · 2020Review
- Mechanism of Ferroptosis and Its Relationships With Other Types of Programmed Cell Death: Insights for Potential Interventions After Intracerebral Hemorrhage.Frontiers in neuroscience · 2020Review
- Programmed Cell Deaths and Potential Crosstalk With Blood-Brain Barrier Dysfunction After Hemorrhagic Stroke.Frontiers in cellular neuroscience · 2020Article
- The Neuroprotective Effects of Necrostatin-1 on Subarachnoid Hemorrhage in Rats Are Possibly Mediated by Preventing Blood-Brain Barrier Disruption and RIP3-Mediated Necroptosis.Cell transplantation · 2019Article
- An Update On Medical Treatment for Intracerebral Hemorrhage.Translational stroke research · 2018Article
- Alterations in necroptosis during ALDH2‑mediated protection against high glucose‑induced H9c2 cardiac cell injury.Molecular medicine reports · 2018Article
- Neuronal Cell Death.Physiological reviews · 2018Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis was recently discovered as one form of programmed cell death (PCD) and could be specifically inhibited by necrostatin-1. The aim of this study was to examine the effect of necrostatin-1 on brain injury and investigate the role of necrostatin-1 on the other two types PCD (apoptosis and autophagic cell death) in a mouse intracerebral hemorrhage (ICH) model. Male ICR mice received an infusion of type IV collagenase to induce ICH or saline as control into the left striatum. In the presence of vehicle, 3-MA, zVAD, and necrostatin-1 were pretreated with a single intracerebroventricular (i.c.v.) injection in the ipsilateral ventricle 15 min before ICH, respectively. Compared with vehicle groups, necrostatin-1 treatment significantly reduced injury volume and propidium iodide-positive cells at 24 and 72 h after ICH. Immunoblotting analysis showed that necrostatin-1 treatment suppressed autophagic-associated proteins (LC3-II, Beclin-1) and maintained p62 at normal level at 24 and 72 h after ICH. In addition, necrostatin-1 treatment enhanced the protein level of Bcl-2 and decreased the protein level of cleaved caspase-3 and the Beclin-1/Bcl-2 ratio at 24 and 72 h after ICH. Moreover, both 3-MA and necrostatin-1 treatment could suppress cleaved caspase-3 and LC3-II production, whereas zVAD treatment could inhibit caspase-3 cleavage but increased LC3-II protein levels at 72 h after ICH. Taken together, the data demonstrated for the first time that the specific inhibitor necrostatin-1 suppressed apoptosis and autophagy to exert these neuroprotective effects after ICH and that there existed a cross-talk among necroptosis, apoptosis, and autophagy after ICH.
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