ArticleMolecular neurobiology2018
Estrogen Attenuates Local Inflammasome Expression and Activation after Spinal Cord Injury.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 117 citations in OpenAlex.
- The Role of Interleukin-18 After Spinal Cord Injury: Mechanisms and Therapeutic Potential.Cells · 2026Review
- Blood-spinal cord barrier disruption after spinal cord injury: a time-dependent mechanistic review.Frontiers in cellular neuroscience · 2026Review
- A Review of the Potential Use of Antioxidants in Spinal Cord Injuries.Antioxidants (Basel, Switzerland) · 2025Review
- Pectolinarin Promotes Functional Recovery after Spinal Cord Injury by Regulating Microglia Polarization Through the PI3K/AKT Signaling Pathway.Molecular neurobiology · 2025Article
- PDE10A Inhibition Reduces NLRP3 Activation and Pyroptosis in Sepsis and Nerve Injury.International journal of molecular sciences · 2025Article
- Sex Differences in the Regulation of Interleukins in Chronic Pain: A Widely Recognized but Difficult-to-Tackle Factor.International journal of molecular sciences · 2025Review
- Hormonal regulatory networks in spinal cord injury: mechanistic insights, crosstalk, and therapeutic innovations.Frontiers in endocrinology · 2025Review
- Estrogen Alleviates Myocardial Ischemia-Reperfusion Injury by Inhibiting NLRP3 Inflammasome-Mediated Pyroptosis.Cardiology research and practice · 2025Article
- Crosstalk Between Cell Death and Spinal Cord Injury: Neurology and Therapy.Molecular neurobiology · 2024Review
- Sex-specific alterations in functional connectivity and network topology in patients with degenerative cervical myelopathy.Scientific reports · 2024Article
- Spinal Cord Injury Model Mitochondria Connect Altered Function with Defects of Mitochondrion Morphology: an Ultrastructural Study.Molecular neurobiology · 2024Article
- Extracellular vesicles for neural regeneration after spinal cord injury.Neural regeneration research · 2024Article
- The research landscape of immunology research in spinal cord injury from 2012 to 2022.JOR spine · 2023Article
- A comprehensive look at the psychoneuroimmunoendocrinology of spinal cord injury and its progression: mechanisms and clinical opportunities.Military Medical Research · 2023Review
- IL1RAP Knockdown in LPS-Stimulated Normal Human Astrocytes Suppresses LPS-Induced Reactive Astrogliosis and Promotes Neuronal Cell Proliferation.Neurochemical research · 2023Article
- Article
- Advances in molecular therapies for targeting pathophysiology in spinal cord injury.Expert opinion on therapeutic targets · 2023Review
- Estradiol reduction through aromatase inhibition impairs cocaine seeking in male rats.Frontiers in behavioral neuroscience · 2023Article
- An emerging role of inflammasomes in spinal cord injury and spinal cord tumor.Frontiers in immunology · 2023Review
- Inflammasomes as biomarkers and therapeutic targets in traumatic brain injury and related-neurodegenerative diseases: A comprehensive overview.Neuroscience and biobehavioral reviews · 2023Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
17-estradiol (E2) is a neuroprotective hormone with a high anti-inflammatory potential in different neurological disorders. The inflammatory response initiated by spinal cord injury (SCI) involves the processing of interleukin-1beta (IL-1b) and IL-18 mediated by caspase-1 which is under the control of an intracellular multiprotein complex called inflammasome. We recently described in a SCI model that between 24 and 72 h post-injury, most of inflammasome components including IL-18, IL-1b, NLRP3, ASC, and caspase-1 are upregulated. In this study, we investigated the influence of E2 treatment after spinal cord contusion on inflammasome regulation. After contusion of T9 spinal segment, 12-week-old male Wistar rats were treated subcutaneously with E2 immediately after injury and every 12 h for the next 3 days. Behavioral scores were significantly improved in E2-treated animals compared to vehicle-treated groups. Functional improvement in E2-treated animals was paralleled by the attenuated expression of certain inflammasome components such as ASC, NLRP1b, and NLRP3 together with IL1b, IL-18, and caspase-1. On the histopathological level, microgliosis and oligodendrocyte injury was ameliorated. These findings support and extend the knowledge of the E2-mediated neuroprotective function during SCI. The control of the inflammasome machinery by E2 might be a missing piece of the puzzle to understand the anti-inflammatory potency of E2.
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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.