ArticleJournal of neuroinflammation2011
S-nitrosoglutathione reduces oxidative injury and promotes mechanisms of neurorepair following traumatic brain injury in rats.
Article in Journal of neuroinflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 103 citations in OpenAlex.
- Propofol Protects the Blood-Brain Barrier After Traumatic Brain Injury by Stabilizing the Extracellular Matrix via Prrx1: From Neuroglioma to Neurotrauma.Neurochemical research · 2024Article
- Oral administration of S-nitroso-L-glutathione (GSNO) provides anti-inflammatory and cytoprotective effects during ocular bacterial infections.Cellular and molecular life sciences : CMLS · 2023Article
- Oxidative stress disrupts the cytoskeleton of spinal motor neurons.Brain and behavior · 2023Article
- Secondary Mechanisms of Neurotrauma: A Closer Look at the Evidence.Diseases (Basel, Switzerland) · 2022Review
- Integrated Proteome and Phosphoproteome Analyses Reveal Early- and Late-Stage Protein Networks of Traumatic Brain Injury.Journal of molecular neuroscience : MN · 2022Article
- Effects of Hyperbaric Oxygen Therapy on Serum Adhesion Molecules, and Serum Oxidative Stress in Patients with Acute Traumatic Brain Injury.Journal of personalized medicine · 2021Article
- The Role of BDNF in Experimental and Clinical Traumatic Brain Injury.International journal of molecular sciences · 2021Review
- Effects of Escitalopram on Endoplasmic Reticulum Stress and Oxidative Stress Induced by Tunicamycin.Frontiers in neuroscience · 2021Article
- Disruption of Midkine gene reduces traumatic brain injury through the modulation of neuroinflammation.Journal of neuroinflammation · 2020Article
- Persistent oppression and simple decompression both exacerbate spinal cord ascorbate levels.International journal of medical sciences · 2020Article
- Osteoimmune Modulation and Guided Osteogenesis Promoted by Barrier Membranes Incorporated with S-Nitrosoglutathione (GSNO) and Mesenchymal Stem Cell-Derived Exosomes.International journal of nanomedicine · 2020Article
- Therapeutic exploitation of the S-nitrosoglutathione/S-nitrosylation mechanism for the treatment of contusion spinal cord injury.Neural regeneration research · 2019Article
- Iron accentuated reactive oxygen species release by NADPH oxidase in activated microglia contributes to oxidative stress in vitro.Journal of neuroinflammation · 2019Article
- Regulation of endothelial barrier integrity by redox-dependent nitric oxide signaling: Implication in traumatic and inflammatory brain injuries.Nitric oxide : biology and chemistry · 2019Article
- Adapting Proteostasis and Autophagy for Controlling the Pathogenesis of Cystic Fibrosis Lung Disease.Frontiers in pharmacology · 2019Review
- Combined treatment with GSNO and CAPE accelerates functional recovery via additive antioxidant activities in a mouse model of TBI.Journal of neuroscience research · 2018Article
- The cysteine-rich whey protein supplement, Immunocal®, preserves brain glutathione and improves cognitive, motor, and histopathological indices of traumatic brain injury in a mouse model of controlled cortical impact.Free radical biology & medicine · 2018Article
- Amelioration of spinal cord injury in rats by blocking peroxynitrite/calpain activity.BMC neuroscience · 2018Article
- GSNO promotes functional recovery in experimental TBI by stabilizing HIF-1α.Behavioural brain research · 2018Article
- Hydroxysafflor Yellow A Shows Protection against PPAROxidative medicine and cellular longevity · 2018Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTraumatic brain injury (TBI) induces primary and secondary damage in both the endothelium and the brain parenchyma, collectively termed the neurovascular unit. While neurons die quickly by necrosis, a vicious cycle of secondary injury in endothelial cells exacerbates the initial injury in the neurovascular unit following TBI. In activated endothelial cells, excessive superoxide reacts with nitric oxide (NO) to form peroxynitrite. Peroxynitrite has been implicated in blood brain barrier (BBB) leakage, altered metabolic function, and neurobehavioral impairment. S-nitrosoglutathione (GSNO), a nitrosylation-based signaling molecule, was reported not only to reduce brain levels of peroxynitrite and oxidative metabolites but also to improve neurological function in TBI, stroke, and spinal cord injury. Therefore, we investigated whether GSNO promotes the neurorepair process by reducing the levels of peroxynitrite and the degree of oxidative injury.
methodsTBI was induced by controlled cortical impact (CCI) in adult male rats. GSNO or 3-Morpholino-sydnonimine (SIN-1) (50 μg/kg body weight) was administered orally two hours following CCI. The same dose was repeated daily until endpoints. GSNO-treated (GSNO group) or SIN-1-treated (SIN-1 group) injured animals were compared with vehicle-treated injured animals (TBI group) and vehicle-treated sham-operated animals (Sham group) in terms of peroxynitrite, NO, glutathione (GSH), lipid peroxidation, blood brain barrier (BBB) leakage, edema, inflammation, tissue structure, axon/myelin integrity, and neurotrophic factors.
resultsSIN-1 treatment of TBI increased whereas GSNO treatment decreased peroxynitrite, lipid peroxides/aldehydes, BBB leakage, inflammation and edema in a short-term treatment (4-48 hours). GSNO also reduced brain infarctions and enhanced the levels of NO and GSH. In a long-term treatment (14 days), GSNO protected axonal integrity, maintained myelin levels, promoted synaptic plasticity, and enhanced the expression of neurotrophic factors.
conclusionOur findings indicate the participation of peroxynitrite in the pathobiology of TBI. GSNO treatment of TBI not only reduces peroxynitrite but also protects the integrity of the neurovascular unit, indicating that GSNO blunts the deleterious effects of peroxynitrite. A long-term treatment of TBI with the same low dose of GSNO promotes synaptic plasticity and enhances the expression of neurotrophic factors. These results support that GSNO reduces the levels of oxidative metabolites, protects the neurovascular unit, and promotes neurorepair mechanisms in TBI.
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