ReviewNeurochemical research2019
Mechanism of Neuroprotection Against Experimental Spinal Cord Injury by Riluzole or Methylprednisolone.
Review in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Spatiotemporal disarray of inflammatory microenvironment following spinal cord injury.Neural regeneration research · 2026Article
- Baicalin and CNS-related diseases: new insights into neuroprotective potentials based on underlying mechanisms.Biochemistry and biophysics reports · 2026Review
- Nanoparticle and epothilone D combinatorial intervention improves motor performance and regeneration in chronic cervical spinal cord injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Early nanoparticle intervention preserves motor function following cervical spinal cord injury.Bioengineering & translational medicine · 2025Article
- Methylprednisolone effects on serum biochemical factors (CRP, PCT, IL-6, TNF-a) in viral pneumonia.Journal of medical biochemistry · 2025Article
- Prospects and challenges in NMDAR signaling in spinal cord injury recovery and neural circuit remodeling.Regenerative therapy · 2025Review
- 50 years of methylprednisolone application in spinal cord injury: a bibliometric analysis.Acta neurochirurgica · 2025Review
- Research Progress on Biomaterials for Spinal Cord Repair.International journal of nanomedicine · 2025Review
- Down-regulation of neuregulin2 (NRG2) following spinal cord injury in C57BL/6 mice: Its implications in therapeutic potential.Iranian journal of basic medical sciences · 2025Article
- Crosstalk Between Cell Death and Spinal Cord Injury: Neurology and Therapy.Molecular neurobiology · 2024Review
- Pharmacological interventions targeting the microcirculation following traumatic spinal cord injury.Neural regeneration research · 2024Review
- Novel Therapeutic Effects in Rat Spinal Cord Injuries: Recovery of the Definitive and Early Spinal Cord Injury by the Administration of Pentadecapeptide BPC 157 Therapy.Current issues in molecular biology · 2022Article
- The immune microenvironment and tissue engineering strategies for spinal cord regeneration.Frontiers in cellular neuroscience · 2022Review
- Development of a New Formulation Based on In Situ Photopolymerized Polymer for the Treatment of Spinal Cord Injury.Polymers · 2021Article
- Valproic Acid: A Potential Therapeutic for Spinal Cord Injury.Cellular and molecular neurobiology · 2021Review
- GABAergic Mechanisms Can Redress the Tilted Balance between Excitation and Inhibition in Damaged Spinal Networks.Molecular neurobiology · 2021Review
- Dexpramipexole Enhances KMolecular neurobiology · 2021Article
- Acute spinal cord injury: Pathophysiology and pharmacological intervention (Review).Molecular medicine reports · 2021Review
- Cenobamate: Neuroprotective Potential of a New Antiepileptic Drug.Neurochemical research · 2021Review
- Melatonin Synergizes With Methylprednisolone to Ameliorate Acute Spinal Cord Injury.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Any spinal cord injury carries the potential for persistent disability affecting motor, sensory and autonomic functions. To prevent this outcome, it is highly desirable to block a chain of deleterious reactions developing in the spinal areas immediately around the primary lesion. Thus, early timing of pharmacological neuroprotection should be one major strategy whose impact may be first studied with preclinical models. Using a simple in vitro model of the rat spinal cord it is possible to mimic pathological processes like excitotoxicity that damages neurons because of excessive glutamate receptor activation due to injury, or hypoxic/dysmetabolic insult that preferentially affects glia following vascular dysfunction. While ongoing research is exploring the various components of pathways leading to cell death, current treatment principally relies on the off-label use of riluzole (RLZ) or methylprednisolone sodium succinate (MPSS). The mechanism of action of these drugs is diverse as RLZ targets mainly neurons and MPSS targets glia. Even when applied after a transient excitotoxic stimulus, RLZ can provide effective prevention of secondary excitotoxic damage to premotoneurons, although not to motoneurons that remain very vulnerable. This observation indicates persistent inability to express locomotor activity despite pharmacological treatment conferring some histological protection. MPSS can protect glia from dysmetabolic insult, yet it remains poorly effective to prevent neuronal death. In summary, it appears that these pharmacological agents can produce delayed protection for certain cell types only, and that their combined administration does not provide additional benefit. The search should continue for better, mechanism-based neuroprotective agents.
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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.