scholarly journals Therapeutic time window for the effects of erythropoietin on astrogliosis and neurite outgrowth in an in vitro model of spinal cord injury

Medicine ◽  
2018 ◽  
Vol 97 (9) ◽  
pp. e9913 ◽  
Author(s):  
Hea Nam Hong ◽  
Ju Hee Shim ◽  
You Jin Won ◽  
Jong Yoon Yoo ◽  
Chang Ho Hwang
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neurite Outgrowth ◽  
In Vitro Model ◽  
Time Window ◽  
Cord Injury ◽  
Vitro Model ◽  
Therapeutic Time Window

The development of a rat in vitro model of spinal cord injury demonstrating the additive effects of rho and ROCK inhibitors on neurite outgrowth and myelination

Glia ◽  
2011 ◽  
Vol 60 (3) ◽  
pp. 441-456 ◽  
Author(s):  
Stephanie D. Boomkamp ◽  
Mathis O. Riehle ◽  
Jenifer Wood ◽  
Michael F. Olson ◽  
Susan C. Barnett
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neurite Outgrowth ◽  
In Vitro Model ◽  
Additive Effects ◽  
Cord Injury ◽  
Vitro Model

scholarly journals Gal-3 is a potential biomarker for spinal cord injury and Gal-3 deficiency attenuates neuroinflammation through ROS/TXNIP/NLRP3 signaling pathway

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Zhouliang Ren ◽  
Weidong Liang ◽  
Jun Sheng ◽  
Chuanhui Xun ◽  
Tao Xu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Signaling Pathway ◽  
In Vitro Model ◽  
Sd Rat ◽  
Potential Biomarker ◽  
Cord Injury ◽  
Vitro Model

Abstract Spinal cord injury (SCI) often occurs in young and middle-aged population. The present study aimed to clarify the function of Galectin-3 (Gal-3) in neuroinflammation of SCI. Sprague–Dawley (SD) rat models with SCI were established in vivo. PC12 cell model in vitro was induced by lipopolysaccharide (LPS). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Gene chip were used to analyze the expression levels of genes in the signaling pathway. Histological assessment, ELISA and Western blotting were conducted to evaluate the effects of Gal-3 upon the SCI model. In the in vivo SD rat model, Gal-3 expression level was up-regulated. The inhibition of Gal-3 attenuated the neuroinflammation in SCI model. The inhibition of Gal-3 could also mitigate the neuroinflammation and reactive oxygen species (ROS) in in vitro model. ROS reduced the effect of Gal-3 on oxidative stress in in vitro model. Down-regulating the content of TXNIP decreased the effect of Gal-3 on neuroinflammation in in vitro model. Suppressing the level of NLRP3 could weaken the effect of Gal-3 on neuroinflammation in in vitro model. Our data highlight that the Gal-3 plays a vital role in regulating the severity of neuroinflammation of SCI by enhancing the activation of ROS/TXNIP/NLRP3 signaling pathway. In addition, inflammasome/IL-1β production probably acts as the therapeutic target in SCI.

ASIC channel inhibition enhances excitotoxic neuronal death in an in vitro model of spinal cord injury

Neuroscience ◽  
2017 ◽  
Vol 343 ◽  
pp. 398-410 ◽  
Author(s):  
Graciela L. Mazzone ◽  
Priyadharishini Veeraraghavan ◽  
Carlota Gonzalez-Inchauspe ◽  
Andrea Nistri ◽  
Osvaldo D. Uchitel
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neuronal Death ◽  
In Vitro Model ◽  
Channel Inhibition ◽  
Cord Injury ◽  
Excitotoxic Neuronal Death ◽  
Vitro Model

A Functional In Vitro Model for Studying the Cellular and Molecular Basis of Spinal Cord Injury

Spine ◽  
1993 ◽  
Vol 18 (9) ◽  
pp. 1125-1133 ◽  
Author(s):  
Hiroyuki Takeda ◽  
Vincent J. Caiozzo ◽  
Vance O. Gardner
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Molecular Basis ◽  
In Vitro Model ◽  
Cord Injury ◽  
Vitro Model

scholarly journals Pharmacological Suppression of CNS Scarring by Deferoxamine Reduces Lesion Volume and Increases Regeneration in an In Vitro Model for Astroglial-Fibrotic Scarring and in Rat Spinal Cord Injury In Vivo

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0134371 ◽  
Author(s):  
Christina Francisca Vogelaar ◽  
Brigitte König ◽  
Stefanie Krafft ◽  
Veronica Estrada ◽  
Nicole Brazda ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
In Vitro Model ◽  
Lesion Volume ◽  
Rat Spinal Cord ◽  
Cord Injury ◽  
Vitro Model

Review of clinical trials of neuroprotection in acute spinal cord injury

1999 ◽  
Vol 6 (1) ◽  
pp. E10 ◽  
Author(s):  
Charles H. Tator ◽  
Michael G. Fehlings
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Clinical Trials ◽  
Treatment Time ◽  
Time Window ◽  
Current Knowledge ◽  
Acute Spinal Cord Injury ◽  
Randomized Controlled Studies ◽  
Cord Injury ◽  
Therapeutic Time Window

In this paper the authors review the clinical trials of neuroprotection that have been performed for the treatment of acute spinal cord injury (SCI). The biological rationale for the selection of each treatment modality is discussed with reference to current knowledge of the principles in the management of acute SCI as well as the primary and secondary injury mechanisms identified by experimental and clinical studies of the pathophysiology of acute SCI. The trials are evaluated with regard to the availability and use of accurate clinical outcome measures, and the methodologies of the trials are critically evaluated with an emphasis on prospective randomized controlled studies. A detailed description and critical analysis are provided of the results of the 10 clinical trials conducted to date in which a randomized prospective controlled design has been used. The issue of the therapeutic time window in acute SCI is discussed. To date, methylprednisolone is the only effective neuroprotective agent that has been established for use in human SCI, and the only therapeutic time window established in human SCI is a maximum trauma-to-treatment time of 8 hours.

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