ArticleBMC neuroscience2018
Amelioration of spinal cord injury in rats by blocking peroxynitrite/calpain activity.
Article in BMC neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- Exploring Ubiquitination in Spinal Cord Injury Therapy: Multifaceted Targets and Promising Strategies.Neurochemical research · 2025Review
- Mechanisms of Traumatic Spinal Cord Injury AIS Grade Conversion.Neurotrauma reports · 2025Review
- Research Progress of Antioxidants in Oxidative Stress Therapy after Spinal Cord Injury.Neurochemical research · 2023Review
- Time-Dependent Changes in the Bladder Muscle Metabolome After Traumatic Spinal Cord Injury in Rats Using Metabolomics.International neurourology journal · 2023Article
- Association between Cerebrospinal Fluid and Serum Biomarker Levels and Diagnosis, Injury Severity, and Short-Term Outcomes in Patients with Acute Traumatic Spinal Cord Injury.Diagnostics (Basel, Switzerland) · 2023Article
- Neuroprotective effects of Alda-1 mitigate spinal cord injury in mice: involvement of Alda-1-induced ALDH2 activation-mediated suppression of reactive aldehyde mechanisms.Neural regeneration research · 2022Article
- GSNOR and ALDH2 alleviate traumatic spinal cord injury.Brain research · 2021Article
- Role of the Polyol Pathway in Locomotor Recovery and Wallerian Degeneration after Spinal Cord Contusion Injury.Neurotrauma reports · 2021Article
- Therapeutic exploitation of the S-nitrosoglutathione/S-nitrosylation mechanism for the treatment of contusion spinal cord injury.Neural regeneration research · 2019Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSpinal cord injury (SCI) is one of the leading causes of disability and chronic pain. In SCI-induced pathology, homeostasis of the nitric oxide (NO) metabolome is lost. Major NO metabolites such as S-nitrosoglutathione (GSNO) and peroxynitrite are reported to play pivotal roles in regulating the activities of key cysteine proteases, calpains. While peroxynitrite (a metabolite of NO and superoxide) up regulates the activities of calpains leading to neurodegeneration, GSNO (a metabolite of NO and glutathione) down regulates the activities of calpains leading to neuroprotection. In this study, effect of GSNO on locomotor function and pain threshold and their relationship with the levels of peroxynitrite and the activity of calpain in the injured spinal cord were investigated using a 2-week rat model of contusion SCI.
resultsSCI animals were initially treated with GSNO at 2 h after the injury followed by a once daily dose of GSNO for 14 days. Locomotor function was evaluated by "Basso Beattie and Bresnahan (BBB) locomotor rating scale" and pain by mechanical allodynia. Peroxynitrite level, as expression of 3-nitrotyrosine (3-NT), calpain activity, as the degradation products of calpain substrate alpha II spectrin, and nNOS activity, as the expression phospho nNOS, were measured by western blot analysis. Treatment with GSNO improved locomotor function and mitigated pain. The treatment also reduced the levels of peroxynitrite (3-NT) and decreased activity of calpains. Reduced levels of peroxynitrite resulted from the GSNO-mediated inhibition of aberrant activity of neuronal nitric oxide synthase (nNOS).
conclusionsThe data indicates that higher levels of 3-NT and aberrant activities of nNOS and calpains correlated with SCI pathology and functional deficits. Treatment with GSNO improved locomotor function and mitigated mechanical allodynia acutely post-injury. Because GSNO shows potential to ameliorate experimental SCI, we discuss implications for GSNO therapy in clinical SCI research.
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