ArticleCellular and molecular neurobiology2014
Neuroprotection induced by N-acetylcysteine and selenium against traumatic brain injury-induced apoptosis and calcium entry in hippocampus of rat.
Article in Cellular and molecular neurobiology, 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, 89 citations in OpenAlex.
- Combined clemastine fumarate and selenomethionine promote remyelination via PI3K/Akt/mTOR signaling in experimental multiple sclerosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Endoplasmic Reticulum-Mitochondrial Crosstalk in Calcium Regulation: Mechanistic Insights and Therapeutic Implications in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Neurological Manifestations Following Traumatic Brain Injury: Role of Behavioral, Neuroinflammation, Excitotoxicity, Nrf-2 and Nitric Oxide.CNS & neurological disorders drug targets · 2025Review
- N-Acetylcysteine and Probenecid Adjuvant Therapy for Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- The Interplay of Oxidative Stress and ROS Scavenging: Antioxidants as a Therapeutic Potential in Sepsis.Vaccines · 2022Review
- Suitability of Banana and Plantain Fruits in Modulating Neurodegenerative Diseases: Implicating the In Vitro and In Vivo Evidence from Neuroactive Narratives of Constituent Biomolecules.Foods (Basel, Switzerland) · 2022Review
- Polydopamine nanoparticles attenuate retina ganglion cell degeneration and restore visual function after optic nerve injury.Journal of nanobiotechnology · 2021Article
- Selenium-containing protein from selenium-enrichedPharmaceutical biology · 2021Article
- Targeting Oxidative Stress with Antioxidant Duotherapy after Experimental Traumatic Brain Injury.International journal of molecular sciences · 2021Article
- ROS/TNF-α Crosstalk Triggers the Expression of IL-8 and MCP-1 in Human Monocytic THP-1 Cells via the NF-κB and ERK1/2 Mediated Signaling.International journal of molecular sciences · 2021Article
- The protective role of selenium against dental amalgam-induced intracellular oxidative toxicity through the TRPV1 channel in DBTRG glioblastoma cells.Journal of applied oral science : revista FOB · 2021Article
- Effects of myricetin against cadmium-induced neurotoxicity in PC12 cells.Toxicology research · 2021Article
- Toxic Peptide FromFrontiers in pharmacology · 2021Article
- Therapeutic Potential of Selenium in Glioblastoma.Frontiers in neuroscience · 2021Review
- N-acetyl cysteine treatment preserves mitochondrial indices of functionality in the brain of hyperammonemic mice.Clinical and experimental hepatology · 2020Article
- Selenium and Neurological Diseases: Focus on Peripheral Pain and TRP Channels.Current neuropharmacology · 2020Review
- Endoplasmic reticulum stress induces apoptosis of arginine vasopressin neurons in central diabetes insipidus via PI3K/Akt pathway.CNS neuroscience & therapeutics · 2019Article
- Traumatic Brain Injury Altered Normal Brain Signaling Pathways: Implications for Novel Therapeutics Approaches.Current neuropharmacology · 2019Article
- Selenium Status Is Not Associated with Cognitive Performance: A Cross-Sectional Study in 154 Older Australian Adults.Nutrients · 2018Article
- Role of Cerium Oxide Nanoparticles in a Paraquat-Induced Model of Oxidative Stress: Emergence of Neuroprotective Results in the Brain.Journal of molecular neuroscience : MN · 2018Article
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4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurodegeneration associated with acute central nervous system injuries and diseases such as spinal cord injury and traumatic brain injury (TBI) are reported to be mediated by the regulation of apoptosis and oxidative stress through Ca(2+) influx. The thiol redox system antioxidants, such as N-acetylcysteine (NAC) and selenium (Se), display neuroprotective activities mediated at least in part by their antioxidant and anti-inflammatory properties. However, there are no reports on hippocampal apoptosis, cytosolic reactive oxygen species (ROS), or Ca(2+) values in rats with an induced TBI. Therefore, we tested the effects of Se and NAC administration on apoptosis, oxidative stress, and Ca(2+) influx through TRPV1 channel activations in the hippocampus of TBI-induced rats. The 32 rats were divided into four groups: control, TBI, TBI + NAC, and TBI + Se groups. Intraperitoneal administrations of NAC and Se were performed at 1, 24, 48, and 72 h after TBI induction. After 3 days, the hippocampal neurons were freshly isolated from the rats. In cytosolic-free Ca(2+) analyses, the neurons were stimulated with the TRPV1 channel agonist capsaicin, a pungent compound found in hot chili peppers. Cytosolic-free Ca(2+), apoptosis, cytosolic ROS levels, and caspase-3 and -9 activities were higher in the TBI group than control. The values in the hippocampus were decreased by Se and NAC administrations. In conclusion, we observed that NAC and Se have protective effects on oxidative stress, apoptosis, and Ca(2+) entry via TRPV1 channel activation in the hippocampus of this TBI model, but the effect of NAC appears to be much greater than that of Se. They are both interesting candidates for studying the amelioration of TBIs.
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