ArticleMediators of inflammation2008
Inhibitory effect on cerebral inflammatory response following traumatic brain injury in rats: a potential neuroprotective mechanism of N-acetylcysteine.
Article in Mediators of inflammation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 170 citations in OpenAlex.
- Repurposing of high-dose N-acetylcysteine as anti-inflammatory, antioxidant and neuroprotective agent in moderate to severe traumatic brain injury patients: a randomized controlled trial.Inflammopharmacology · 2025Trial
- I-gel Laryngeal Mask Airway Combined with Tracheal Intubation Attenuate Systemic Stress Response in Patients Undergoing Posterior Fossa Surgery.Mediators of inflammation · 2015Trial
- The NLRP3 Inflammasome in Neuropsychiatric Disorders: Molecular Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- A delayed pharmacological treatment strategy attenuates noise-induced tinnitus in rats.Scientific reports · 2026Article
- A Dopamine D1-Like Receptor Agonist Ameliorates Traumatic Brain Injury Through its Immunosuppressive Effects.Cellular and molecular neurobiology · 2026Article
- Coaxial nanofiber design for traumatic brain injury: a review and framework for phase-responsive therapeutics.Discover nano · 2026Review
- Traumatic Brian Injury (TBI) unraveled: molecular disruptions and therapeutic avenues.Inflammopharmacology · 2025Review
- Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- The systemic treatments for drug reaction with eosinophilia and systemic symptoms (DRESS) beyond corticosteroids.The World Allergy Organization journal · 2024Review
- N-acetyl Cysteine Overdose Induced Acute Toxicity and Hepatic Microvesicular Steatosis by Disrupting GSH and Interfering Lipid Metabolisms in Normal Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Elucidating the pivotal molecular mechanisms, therapeutic and neuroprotective effects of lithium in traumatic brain injury.Brain and behavior · 2024Review
- A Modern Approach to the Treatment of Traumatic Brain Injury.Medicines (Basel, Switzerland) · 2024Review
- Treatment effects of N-acetyl cysteine on resting-state functional MRI and cognitive performance in patients with chronic mild traumatic brain injury: a longitudinal study.Frontiers in neurology · 2024Article
- Neuroprotection strategies in traumatic brain injury: Studying the effectiveness of different clinical approaches.Surgical neurology international · 2024Review
- Better together? Treating traumatic brain injury with minocycline plus N-acetylcysteine.Neural regeneration research · 2022Review
- Stress- and drug-induced neuroimmune signaling as a therapeutic target for comorbid anxiety and substance use disorders.Pharmacology & therapeutics · 2022Review
- Targeting Molecular Mediators of Ferroptosis and Oxidative Stress for Neurological Disorders.Oxidative medicine and cellular longevity · 2022Review
- Antioxidant therapies in traumatic brain injury.Neurochemistry international · 2022Article
- Delayed dosing of minocycline plus N-acetylcysteine reduces neurodegeneration in distal brain regions and restores spatial memory after experimental traumatic brain injury.Experimental neurology · 2021Article
- Targeting Oxidative Stress with Antioxidant Duotherapy after Experimental Traumatic Brain Injury.International journal of molecular sciences · 2021Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although N-acetylcysteine (NAC) has been shown to be neuroprotective for traumatic brain injury (TBI), the mechanisms for this beneficial effect are still poorly understood. Cerebral inflammation plays an important role in the pathogenesis of secondary brain injury after TBI. However, it has not been investigated whether NAC modulates TBI-induced cerebral inflammatory response. In this work, we investigated the effect of NAC administration on cortical expressions of nuclear factor kappa B (NF-kappaB) and inflammatory proteins such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and intercellular adhesion molecule-1 (ICAM-1) after TBI. As a result, we found that NF-kappaB, proinflammatory cytokines, and ICAM-1 were increased in all injured animals. In animals given NAC post-TBI, NF-kappaB, IL-1beta, TNF-alpha, and ICAM-1 were decreased in comparison to vehicle-treated animals. Measures of IL-6 showed no change after NAC treatment. NAC administration reduced brain edema, BBB permeability, and apoptotic index in the injured brain. The results suggest that post-TBI NAC administration may attenuate inflammatory response in the injured rat brain, and this may be one mechanism by which NAC ameliorates secondary brain damage following 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.