scholarly journals Ibuprofen Enhances Recovery from Spinal Cord Injury by Limiting Tissue Loss and Stimulating Axonal Growth

2009 ◽  
Vol 26 (1) ◽  
pp. 81-95 ◽  
Author(s):  
Xingxing Wang ◽  
Stephane Budel ◽  
Kenneth Baughman ◽  
Grahame Gould ◽  
Kang-Ho Song ◽  
...  
Author(s):  
Olivia H. Bodart ◽  
Ethan P. Glaser ◽  
Steven M. MacLean ◽  
Meifan A. Chen ◽  
John C. Gensel

Spinal cord injury (SCI) is a life-altering event for which there is no treatment. Depending on injury location and severity, the breadth of the effects can go far past simple mobility. Primary mechanical trauma triggers a variety of secondary cellular events that exacerbate tissue loss as well as facilitate endogenous repair. A large focus of SCI research is on understanding the pathophysiological mechanisms through which these secondary responses contribute to morbidities associated with SCI. Neuroinflammation, a common response to central nervous system (CNS) insult, is central to the secondary injury cascade. In the context of SCI, the inflammatory response plays a contradictory role in recovery; immune cells release both pro- and anti-inflammatory cytokines at the injury site and clear debris while also causing damage to spared tissue. The major innate and adaptive immune cells that respond to SCI are neutrophils, astrocytes, microglia/macrophages, B cells, and T cells. For each cell type, the timing of the cellular response (in both human and rodent models of SCI), the potential role each cell type plays in the pathophysiology of injury, and the therapeutic implications of targeting each cell type for SCI recovery are discussed.


Neuron ◽  
2014 ◽  
Vol 83 (4) ◽  
pp. 789-796 ◽  
Author(s):  
Paul Lu ◽  
Grace Woodruff ◽  
Yaozhi Wang ◽  
Lori Graham ◽  
Matt Hunt ◽  
...  

2020 ◽  
Author(s):  
Qi Liao ◽  
Jiang-Hua Ming ◽  
Ge-Liang Hu

Abstract Background: As exosomes have been confirmed as a reservoir of siRNAs involved in certain diseases, the current study aims to investigate whether exosomal-siRNA could exert a protective role in spinal cord injury (SCI). Methods and Results: Exosomes in our experiment were isolated from lysosomal membrane-associated protein 2b (Lamp2b) overexpression HEK 293T cells, and purity of exosomes was characterized by the expression of CD9, CD47, and CD63 via western blot. Furthermore, the siRNA pool contains four siRNAs including siRNA-NgR, siRNA-LINGO-1, siRNA-Troy, and siRNA-PTEN was loaded to the exosomes, which indicated a significant role for the siRNA pool in reducing the expression of axon growth inhibitory factors. Upon the completion of loading into exosomes (exo-siRNA pool), the exo-siRNA pool was injected into primary cortical neurons of the SCI model in rats before cell proliferation and Rho expression were determined With the results revealed that purified addition could be applied to future experiments. The exo-siRNA pooled transfection caused downregulation of axon growth suppressors in primary cortical neurons including Nogo receptors (NgR), leucine-rich repeats and immunoglobulin domain-containing protein 1 (LINGO-1), Troy, and phosphatase and tenson homolog (PTEN). Cell proliferation and Rho expression of primary cortical neurons inhibited the expression of axonal growth inhibitors in rats with SCI by transfecting exogenous Sirna. Conclusion: This study confirmed that exosomes derived from Lamp2b overexpression HEK 293T cells facilitated both the recovery of functions and the survival of neurons when being loaded with the siRNA pool.


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