Review for "Novel circular RNA 2960 contributes to secondary damage of spinal cord injury by sponging miRNA ‐124"

2020 ◽  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Secondary Damage ◽  
Cord Injury

scholarly journals Does dexmedetomidine reduce secondary damage after spinal cord injury? An experimental study

2009 ◽  
Vol 18 (3) ◽  
pp. 336-344 ◽  
Author(s):  
Adem Aslan ◽  
Mustafa Cemek ◽  
Olcay Eser ◽  
Korhan Altunbaş ◽  
Mehmet Emin Buyukokuroglu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Experimental Study ◽  
Spinal Cord Injury ◽  
Secondary Damage ◽  
Cord Injury

scholarly journals Chirality-Dependent Anti-Inflammatory Effect of Glutathione after Spinal Cord Injury in an Animal Model

2021 ◽  
Vol 14 (8) ◽  
pp. 792
Author(s):  
Seong-Jun Kim ◽  
Wan-Kyu Ko ◽  
Gong-Ho Han ◽  
Daye Lee ◽  
Yuhan Lee ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Therapeutic Potential ◽  
Specific Interaction ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Secondary Damage ◽  
Cord Injury ◽  
Mitogen Activated Protein ◽  
Pro Inflammatory Cytokines

Neuroinflammation forms a glial scar following a spinal cord injury (SCI). The injured axon cannot regenerate across the scar, suggesting permanent paraplegia. Molecular chirality can show an entirely different bio-function by means of chiral-specific interaction. In this study, we report that d-chiral glutathione (D-GSH) suppresses the inflammatory response after SCI and leads to axon regeneration of the injured spinal cord to a greater extent than l-chiral glutathione (L-GSH). After SCI, axon regrowth in D-GSH-treated rats was significantly increased compared with that in L-GSH-treated rats (*** p < 0.001). Secondary damage and motor function were significantly improved in D-GSH-treated rats compared with those outcomes in L-GSH-treated rats (** p < 0.01). Moreover, D-GSH significantly decreased pro-inflammatory cytokines and glial fibrillary acidic protein (GFAP) via inhibition of the mitogen-activated protein kinase (MAPK) signaling pathway compared with L-GSH (*** p < 0.001). In primary cultured macrophages, we found that D-GSH undergoes more intracellular interaction with activated macrophages than L-GSH (*** p < 0.001). These findings reveal a potential new regenerative function of chiral GSH in SCI and suggest that chiral GSH has therapeutic potential as a treatment of other diseases.

scholarly journals Effect of carvedilol on secondary damage in experimental spinal cord injury in rats

2014 ◽  
Author(s):  
Yasar Karatas ◽  
Sahika Liva Cengiz ◽  
Hasan Esen ◽  
Aysun Toker ◽  
Cigdem Savas
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Experimental Spinal Cord Injury ◽  
Secondary Damage ◽  
Cord Injury

Novel circular RNA 2960 contributes to secondary damage of spinal cord injury by sponging miRNA ‐124

2020 ◽  
Author(s):  
Jun Chen ◽  
Bin Fu ◽  
Jing Bao ◽  
Rong Su ◽  
Haoning Zhao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Circular Rna ◽  
Secondary Damage ◽  
Cord Injury

scholarly journals CCL3 contributes to secondary damage after spinal cord injury

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Nicolas Pelisch ◽  
Jose Rosas Almanza ◽  
Kyle E. Stehlik ◽  
Brandy V. Aperi ◽  
Antje Kroner
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Lesion Size ◽  
Secondary Injury ◽  
Wild Type ◽  
Locomotor Recovery ◽  
Secondary Damage ◽  
Cord Injury

Abstract Background Secondary damage after spinal cord injury (SCI) is characterized by a cascade of events including hemorrhage, apoptosis, oxidative stress, and inflammation which increase the lesion size which can influence the functional impairment. Thus, identifying specific mechanisms attributed to secondary injury is critical in minimizing tissue damage and improving neurological outcome. In this work, we are investigating the role of CCL3 (macrophage inflammatory protein 1-α, MIP-1α), a chemokine involved in the recruitment of inflammatory cells, which plays an important role in inflammatory conditions of the central and peripheral nervous system. Methods A mouse model of lower thoracic (T11) spinal cord contusion injury was used. We assessed expression levels of CCL3 and its receptors on the mRNA and protein level and analyzed changes in locomotor recovery and the inflammatory response in the injured spinal cord of wild-type and CCL3−/− mice. Results The expression of CCL3 and its receptors was increased after thoracic contusion SCI in mice. We then examined the role of CCL3 after SCI and its direct influence on the inflammatory response, locomotor recovery and lesion size using CCL3−/− mice. CCL3−/− mice showed mild but significant improvement of locomotor recovery, a smaller lesion size and reduced neuronal damage compared to wild-type controls. In addition, neutrophil numbers as well as the pro-inflammatory cytokines and chemokines, known to play a deleterious role after SCI, were markedly reduced in the absence of CCL3. Conclusion We have identified CCL3 as a potential target to modulate the inflammatory response and secondary damage after SCI. Collectively, this study shows that CCL3 contributes to progressive tissue damage and functional impairment during secondary injury after SCI.

Tauroursodeoxycholic acid and secondary damage after spinal cord injury in rats

2008 ◽  
Vol 15 (6) ◽  
pp. 665-671 ◽  
Author(s):  
Ahmet Çolak ◽  
Bilal Kelten ◽  
Ayhan Sağmanligil ◽  
Osman Akdemir ◽  
Alper Karaoğlan ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Tauroursodeoxycholic Acid ◽  
Secondary Damage ◽  
Cord Injury

scholarly journals Mitogen-Activated Protein Kinase-Activated Protein Kinase 2 (MK2) Contributes to Secondary Damage after Spinal Cord Injury

2010 ◽  
Vol 30 (41) ◽  
pp. 13750-13759 ◽  
Author(s):  
N. Ghasemlou ◽  
R. Lopez-Vales ◽  
C. Lachance ◽  
T. Thuraisingam ◽  
M. Gaestel ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Protein Kinase ◽  
Mitogen Activated Protein Kinase ◽  
Secondary Damage ◽  
Cord Injury ◽  
Mitogen Activated Protein

scholarly journals Prevention, identification, and treatment of perioperative spinal cord injury

2008 ◽  
Vol 25 (5) ◽  
pp. E15 ◽  
Author(s):  
Henry Ahn ◽  
Michael G. Fehlings
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Clinical Outcome ◽  
Clinical Studies ◽  
Basic Science ◽  
Treatment Options ◽  
Arterial Blood ◽  
Secondary Damage ◽  
Increased Risk ◽  
Cord Injury

Object In this report, the authors suggest evidence-based approaches to minimize the chance of perioperative spinal cord injury (POSCI) and optimize outcome in the event of a POSCI. Methods A systematic review of the basic science and clinical literature is presented. Results Authors of clinical studies have assessed intraoperative monitoring to minimize the chance of POSCI. Furthermore, preoperative factors and intraoperative issues that place patients at increased risk of POSCI have been identified, including developmental stenosis, ankylosing spondylitis, preexisting myelopathy, and severe deformity with spinal cord compromise. However, no studies have assessed methods to optimize outcomes specifically after POSCIs. There are a number of studies focussed on the pathophysiology of SCI and the minimization of secondary damage. These basic science and clinical studies are reviewed, and treatment options outlined in this article. Conclusions There are a number of treatment options, including maintenance of mean arterial blood pressure > 80 mm Hg, starting methylprednisolone treatment preoperatively, and multimodality monitoring to help prevent POSCI occurrence, minimize secondary damage, and potentially improve the clinical outcome of after a POSCI. Further prospective cohort studies are needed to delineate incidence rate, current practice patterns for preventing injury and minimizing the clinical consequences of POSCI, factors that may increase the risk of POSCI, and determinants of clinical outcome in the event of a POSCI.

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