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Spinal cord injury (SCI) is a serious problem in the central nervous system resulting in high disability and mortality with complex pathophysiological mechanisms. Oxidative stress is one of the main secondary reactions of SCI, and its main pathophysiological marker is the production of excess reactive oxygen species. The overproduction of reactive...
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... • АФК реагируют с компонентом мембраны, содержащим полиненасыщенные жирные кислоты, акцептируя электрон. Этот электрон связывается с молекулами липидов и генерирует их активные формы; • активируемые формы липидов запускают реакции с участием свободных радикалов, в результате чего генерируется еще большее количество АФК; • продуцируются активные формы других молекул, включая 4-гидроксиноненал и 2-пропенал, оказывающие цитотоксическое действие [16]. Поскольку свободные радикалы недолговечны и трудно оценить их содержание, измеряют концентрацию конечного продукта окисления липидов и белков в реакции с тиобарбитуровой кислотой (их называют ТБК-продуктами) -например, малонового диальдегида. ...
Aim. To evaluate changes in the concentration of molecules that mark the neurodegenerative process, experimental spinal cord injuries (SCI) of various origins were studied.
Materials and methods. SCI was modeled in six-month-old male Wistar rats by exposing the T10 vertebra to: carbon dioxide under a pressure of 2 N/cm ² (pneumocontusion); free-falling load of three weights of 1.12 N/cm ² , 1.68 N/cm ² , 1.96 N/cm ² (contusion injury); compression with forceps (compression injury); partial hemisection of the spinal cord; mechanical laminectomy using a mechanical drill. There were 6 rats in each group, including the intact control group. On the 28th day after a single application of SCI in rats, the concentrations of tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), albumin, thiobarbituric acid reactive substances (TBA-RS) and superoxide dismutase activity were assessed in the blood serum.
Results. When modeling SCI of various origins in rats, the serum concentration of TNF-α increased (from 115.5% ( p < 0.05) in mild contusion to 234.5% ( p < 0.05) in compression trauma compared to intact control) as well as IL-6 (from 49.2% ( p < 0.05) in mechanical laminectomy to 89.8% ( p < 0.05) in hemisection compared with intact control), suggesting activation of inflammatory reactions. The concentration of albumin in the blood serum of rats with SCI was lower than that of intact animals, especially in the hemisection group – by 41.9% ( p < 0.05). Animals with SCI had an increase in TBA-RS concentration ranging from 103.2% ( p < 0.05) in mild contusion and compression to 135.5% ( p < 0.05) in pneumocontusion, and a decrease in superoxide dismutase activity ranging from 26.3% ( p < 0.05) in laminectomy to 31.7% ( p < 0.05) in hemisection. At the same time, injuries caused by spinal compression and hemisection led to a more pronounced activation of the inflammatory process, as evidenced by the increased TNF-α content compared to other variants of SCI modeling.
Conclusion. All SCI simulations resulted in equivalent activation of oxidative stress, while inflammation is more pronounced when reproducing compression injury and injury caused by spinal hemisection.
... This results in the initiation of oxidative stress responses [9][10][11] , causing dysfunction in cells at the injury site and the migration and in ltration of in ammatory cells, thereby exacerbating local in ammation. Additionally, it leads to DNA fragmentation, mitochondrial damage, the generation and release of apoptotic factors, ultimately promoting cell apoptosis [10][11][12] . Studies suggest that the excessive production of ROS and lipid peroxidation are among the key mechanisms driving oxidative stress damage following SCI [10,11] . ...
... Studies suggest that the excessive production of ROS and lipid peroxidation are among the key mechanisms driving oxidative stress damage following SCI [10,11] . Inhibiting oxidative stress reactions post-SCI can alleviate secondary SCI and promote functional recovery [12,13] . However, comprehensive research on oxidative stress in SCI is still lacking. ...
Spinal cord injury (SCI) induces oxidative stress reactions, exacerbating secondary damage. Moderating oxidative stress after SCI holds paramount significance for alleviating secondary injury. At the same time, comprehensive investigations into the pathogenesis of oxidative stress in SCI remain limited. In this study, we analyzed public datasets to identify differentially expressed oxidative stress-related genes (DEOSRGs) at various post-injury time points, identifying 25 hub oxidative stress-related genes (OSRGs). We also conducted tests and validations to ascertain the temporal expression patterns of some hub genes at both the tissue and single-cell levels. Subsequently, we unveiled the association between these hub genes and immune cell infiltration. Functional and pathway enrichment analyses were conducted on DEOSRGs at distinct time points, revealing alterations in enriched functions and signaling pathways. Additionally, we summarized potential communication signaling characteristics related to oxidative stress among different cells at various time points at the single-cell level, along with associated ligand-receptor pairs. As a subsequent step, we constructed mRNA-miRNA/mRNA-miRNA-lncRNA regulatory networks related to oxidative stress in SCI and analyzed transcription factors associated with hub OSRGs. Finally, leveraging the DSigDB database, we predicted compounds capable of inhibiting eight hub genes, offering potential drugs or molecules for targeted interventions in oxidative stress following SCI. Consequently, this study holds significance for gaining deeper insights into oxidative stress mechanisms after SCI and timely targeted interventions in oxidative stress following SCI.
Spinal cord injury (SCI) disrupts nerve pathways and affects sensory, motor, and autonomic function. There is currently no effective treatment for SCI. SCI occurs within three temporal periods: acute, subacute, and chronic. In each period there are different alterations in the cells, inflammatory factors, and signaling pathways within the spinal cord. Many biomaterials have been investigated in the treatment of SCI, including hydrogels and fiber scaffolds, and some progress has been made in the treatment of SCI using multiple materials. However, there are limitations when using individual biomaterials in SCI treatment, and these limitations can be significantly improved by combining treatments with stem cells. In order to better understand SCI and to investigate new strategies for its treatment, several combination therapies that include materials combined with cells, drugs, cytokines, etc. are summarized in the current review.
