ArticleNeuromolecular medicine2017
Involvement of IL-17 in Secondary Brain Injury After a Traumatic Brain Injury in Rats.
Article in Neuromolecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 62 citations in OpenAlex.
- Inflammatory blood-based biomarkers to aid in the assessment and prognostication of traumatic brain injury: a TRACK-TBI study.Journal of neuroinflammation · 2026Article
- The Role of Cytokines in Traumatic Brain Injury.Biomedicines · 2026Review
- Th17 cells and IL-17A in traumatic brain injury: mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Inhibition of IL-17 Alleviates Blood-Brain Barrier Disruption Following Diffuse Axonal Injury Accompanied by Hyperglycemia Through the NF-κB Pathway.Mediators of inflammation · 2026Article
- T Cell Involvement in Neuroinflammation After Traumatic Brain Injury: Implications for Therapeutic Intervention.CNS neuroscience & therapeutics · 2025Review
- IL-23 promotes neuronal ferroptosis via IL-23R/STAT3 signaling after traumatic brain injury.Cell communication and signaling : CCS · 2025Article
- Adaptive Immune Dyshomeostasis as a Mediator of Vascular Cognitive Decline: Unraveling Neurovascular Crosstalk.Aging and disease · 2025Review
- The immunological landscape of traumatic brain injury: insights from pathophysiology to experimental models.Frontiers in neurology · 2025Review
- Bioinformatics analysis of G protein subunit gamma transduction protein 2-autophagy axis in CD11b+ dendritic cells as a potential regulator to skew airway neutrophilic inflammation in asthma endotypes.Immunity, inflammation and disease · 2024Article
- Early biomarkers in the presymptomatic phase of cognitive impairment: changes in the endocannabinoidome and serotonergic pathways in Alzheimer's-prone mice after mTBI.Acta neuropathologica communications · 2024Article
- Influence of the brain‑gut axis on neuroinflammation in cerebral ischemia‑reperfusion injury (Review).International journal of molecular medicine · 2024Review
- Emerging Neuroprotective Strategies: Unraveling the Potential of HDAC Inhibitors in Traumatic Brain Injury Management.Current neuropharmacology · 2024Review
- Neutrophil-derived interleukin-17A participates in neuroinflammation induced by traumatic brain injury.Neural regeneration research · 2023Article
- Central role for neurally dysregulated IL-17A in dynamic networks of systemic and local inflammation in combat casualties.Scientific reports · 2023Article
- Mild-to-severe traumatic brain injury in children: altered cytokines reflect severity.Journal of neuroinflammation · 2022Article
- Endogenous Interleukin-17a Contributes to Normal Spatial Memory Retention but Does Not Affect Early Behavioral or Neuropathological Outcomes after Experimental Traumatic Brain Injury.Neurotrauma reports · 2022Article
- γδ T Cell in Cerebral Ischemic Stroke: Characteristic, Immunity-Inflammatory Role, and Therapy.Frontiers in neurology · 2022Review
- Periodontitis Salivary Microbiota Aggravates Ischemic Stroke Through IL-17A.Frontiers in neuroscience · 2022Article
- Emerging Roles of T Helper Cells in Non-Infectious Neuroinflammation: Savior or Sinner.Frontiers in immunology · 2022Review
- Interleukin-17A Mediates Hippocampal Damage and Aberrant Neurogenesis Contributing to Epilepsy-Associated Anxiety.Frontiers in molecular neuroscience · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pro-inflammatory activity of interleukin 17, which is produced by the IL-23/IL-17 axis, has been associated with the pathogenesis of traumatic brain injury (TBI). The study investigated the potential role of IL-17 in secondary brain injury of TBI in a rat model. Our data showed that the levels of IL-17 increased from 6 h to 7 days and peaked at 3 days, in both the CNS and serum, which were consistent with the severity of secondary brain injury. The IL-23 inhibitor suberoylanilide hydroxamic acid (SAHA) treatment markedly decreased the expressions of IL-17 and apoptosis-associated proteins cleaved caspase-3 and increased the protein ratio of Bcl-2 (B cell lymphoma/leukemia-2)/Bax (Bcl-2-associated X protein). Meanwhile, neuronal apoptosis was reduced, and neural function was improved after SAHA treatment. This study suggests that IL-17 is involved in secondary brain injury after TBI. Administering an IL-23 inhibitor and thereby blocking the IL-23/IL-17 axis may be beneficial in the treatment of TBI.
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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.