ArticleNeuropsychiatric disease and treatment2018
The microglial activation profile and associated factors after experimental spinal cord injury in rats.
Article in Neuropsychiatric disease and treatment, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Gasotransmitters in the regulation of connexins in central and peripheral nervous system injuries.Medical gas research · 2027Review
- The Impact of Nuclear Factor Kappa B on the Response of Microglia in Spinal Cord Injuries.Cureus · 2025Review
- Induction of Neural Differentiation and Protection by a Novel Slow-Release Nanoparticle Estrogen Construct in a Rat Model of Spinal Cord Injury.Neurochemical research · 2024Article
- Timed sulfonylurea modulation improves locomotor and sensory dysfunction following spinal cord injury.Frontiers in pharmacology · 2024Article
- Nanomaterials as therapeutic agents to modulate astrocyte-mediated inflammation in spinal cord injury.Materials today. Bio · 2023Review
- Effects of Whole-Body Vibration and Manually Assisted Locomotor Therapy on Neurotrophin-3 Expression and Microglia/Macrophage Mobilization Following Thoracic Spinal Cord Injury in Rats.Current issues in molecular biology · 2023Article
- More attention on glial cells to have better recovery after spinal cord injury.Biochemistry and biophysics reports · 2021Review
- MicroRNAs in the Spinal Microglia Serve Critical Roles in Neuropathic Pain.Molecular neurobiology · 2021Review
- The Potential Role of Inflammation in Modulating Endogenous Hippocampal Neurogenesis After Spinal Cord Injury.Frontiers in neuroscience · 2021Review
- Relationship Between Serum Fibrinogen Level and Depressive Symptoms in an Adult Population with Spinal Cord Injury: A Cross-Sectional Study.Neuropsychiatric disease and treatment · 2021Article
- Inhibition of leucine-rich repeats and calponin homology domain containing 1 accelerates microglia-mediated neuroinflammation in a rat traumatic spinal cord injury model.Journal of neuroinflammation · 2020Article
- Therapeutic Hypothermia Improves Hind Limb Motor Outcome and Attenuates Oxidative Stress and Neuronal Damage in the Lumbar Spinal Cord Following Cardiac Arrest.Antioxidants (Basel, Switzerland) · 2020Article
- Cytokine Profile As a Marker of Cell Damage and Immune Dysfunction after Spinal Cord Injury.Acta naturaeArticle
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSpinal cord injury (SCI) has imposed a great impact on the quality of life of patients due to its relatively young age of onset. The pathophysiology of SCI has been proven to be complicated. Microglia plays an important role in neuroinflammation and second injuries after SCI. Different environment and other factors may determine the microglial activation profile and what role they play. However, neither accurate time-course profiles of microglial activation nor influence factors have been demonstrated in varied SCI models.
methodsA rat compressive SCI model was used. Microglial activation profile and contents of inflammatory factors including IL-1β, IL-6 and TNF-α were detected. Myelination status as well as levels of iron and glutamate concentration, adenosine triphosphate (ATP) and potassium are also assessed.
resultsOur results showed that the activated microglia participating in immune-mediated responses peaked at day 7 post SCI and gradually decreased during the following 3 weeks. Contrarily, myelination and oligodendroglia showed an opposite trend, indicating that microglia may be a key factor partly through inflammatory reaction. Iron and glutamate concentration were found to be the highest at day 7 after SCI while both ATP and potassium reached a low valley at the same time.
conclusionThese findings showed a microglial activation profile and the alterations of associated factors after experiment SCI model. Moreover, our data suggest that high iron and glutamate concentration may be released by damaged oligodendroglia and contribute to the activation of microglial after SCI.
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