ArticleJournal of neuroinflammation2012
Indomethacin protects rats from neuronal damage induced by traumatic brain injury and suppresses hippocampal IL-1β release through the inhibition of Nogo-A expression.
Article in Journal of neuroinflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 34 citations in OpenAlex.
- Traumatic Brian Injury (TBI) unraveled: molecular disruptions and therapeutic avenues.Inflammopharmacology · 2025Review
- Review
- Nature vs. Manmade: Comparing Exosomes and Liposomes for Traumatic Brain Injury.The AAPS journal · 2023Review
- Neuroinflammatory Cytokine Response, Neuronal Death, and Microglial Proliferation in the Hippocampus of Rats During the Early Period After Lateral Fluid Percussion-Induced Traumatic Injury of the Neocortex.Molecular neurobiology · 2022Article
- Role of innate inflammation in traumatic brain injury.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Review
- Management of Traumatic Brain Injury: From Present to Future.Antioxidants (Basel, Switzerland) · 2020Review
- A Three-Day Consecutive Fingolimod Administration Improves Neurological Functions and Modulates Multiple Immune Responses of CCI Mice.Molecular neurobiology · 2017Article
- Pharmacological approaches to intervention in hypomyelinating and demyelinating white matter pathology.Neuropharmacology · 2016Review
- The anti-inflammatory properties of Satureja khuzistanica Jamzad essential oil attenuate the effects of traumatic brain injuries in rats.Scientific reports · 2016Article
- Treatment of traumatic brain injury with anti-inflammatory drugs.Experimental neurology · 2016Review
- Hippocampal Neurophysiologic Changes after Mild Traumatic Brain Injury and Potential Neuromodulation Treatment Approaches.Frontiers in systems neuroscience · 2016Review
- Neuroinflammation in the normal aging hippocampus.Neuroscience · 2015Review
- Novel frontiers in epilepsy treatments: preventing epileptogenesis by targeting inflammation.Expert review of neurotherapeutics · 2013Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNogo-A is a member of the reticulon family of membrane-associated proteins and plays an important role in axonal remodeling. The present study aimed to investigate alterations in Nogo-A expression following traumatic brain injury (TBI)-induced inflammation and neuronal damage.
methodsA weight-drop device was used to deliver a standard traumatic impact to rats. Western blot, RT-PCR and ELISA were used to analyze the expression of Nogo-A and IL-1β. Nogo-A antisense, and an irrelevant control oligonucleotide was intracerebroventricularly infused. We also performed H & E staining and luxol fast blue staining to evaluate the neuronal damage and demyelination resulting from TBI and various treatments.
resultsBased on RT-PCR and western blot analyses, the expression of Nogo-A was found to be significantly upregulated in the hippocampus beginning eight hours after TBI. In addition, TBI caused an apparent elevation in IL-1β levels and severe neuronal damage and demyelination in the tested animals. All of the TBI-associated molecular and cellular consequences could be effectively reversed by treating the animals with the anti-inflammatory drug indomethacin. More importantly, the TBI-associated stimulation in the levels of both Nogo-A and IL-1β could be effectively inhibited by a specific Nogo-A antisense oligonucleotide.
conclusionsOur findings suggest that the suppression of Nogo-A expression appears to be an early response conferred by indomethacin, which then leads to decreases in the levels of IL-1β and TBI-induced neuron damage.
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