scholarly journals Patchouli Alcohol Improves the Integrity of the Blood-Spinal Cord Barrier by Inhibiting Endoplasmic Reticulum Stress Through the Akt/CHOP/Caspase-3 Pathway Following Spinal Cord Injury

2021 ◽  
Vol 9 ◽  
Author(s):  
Chongan Huang ◽  
Weiqi Zhang ◽  
FeiFan Chu ◽  
Hao Qian ◽  
Yining Wang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Neurological Deficits ◽  
Critical Event ◽  
Neuroprotective Effects ◽  
Patchouli Alcohol ◽  
Cord Injury ◽  
Blood Spinal Cord Barrier

Spinal cord injury (SCI) is a destructive and complex disorder of the central nervous system (CNS) for which there is no clinical treatment. Blood-spinal cord barrier (BSCB) rupture is a critical event in SCI that aggravates nerve injury. Therefore, maintaining the integrity of the BSCB may be a potential method to treat SCI. Here, we showed that patchouli alcohol (PA) exerts protective effects against SCI. We discovered that PA significantly prevented hyperpermeability of the BSCB by reducing the loss of tight junctions (TJs) and endothelial cells. PA also suppressed endoplasmic reticulum stress and apoptosis in vitro. Furthermore, in a rat model of SCI, PA effectively improved neurological deficits. Overall, these results prove that PA exerts neuroprotective effects by maintaining BSCB integrity and thus be a promising candidate for SCI treatment.

Deletion of Endoplasmic Reticulum Stress-Induced CHOP Protects Microvasculature Post-Spinal Cord Injury

2012 ◽  
Vol 9 (4) ◽  
pp. 274-281 ◽  
Author(s):  
Janelle M. Fassbender ◽  
Sujata Saraswat-Ohri ◽  
Scott A. Myers ◽  
Mark J. Gruenthal ◽  
Richard L. Benton ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cord Injury

Necrostatin-1 Mitigates Endoplasmic Reticulum Stress After Spinal Cord Injury

2017 ◽  
Vol 42 (12) ◽  
pp. 3548-3558 ◽  
Author(s):  
Shuang Wang ◽  
Jin Wu ◽  
Yu-Zhe Zeng ◽  
Song-Song Wu ◽  
Guo-Rong Deng ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cord Injury

Role of the blood-spinal cord barrier in posttraumatic syringomyelia

2009 ◽  
Vol 11 (6) ◽  
pp. 696-704 ◽  
Author(s):  
Sarah J. Hemley ◽  
B. Biotech ◽  
Jian Tu ◽  
Marcus A. Stoodley
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Amino Acid ◽  
Vascular Permeability ◽  
Neurological Deficits ◽  
Time Points ◽  
Functional Integrity ◽  
Cord Injury ◽  
Posttraumatic Syringomyelia ◽  
Blood Spinal Cord Barrier

Object Posttraumatic syringomyelia produces a significant burden of pain and neurological deficits in patients with spinal cord injury. The mechanism of syrinx formation is unknown and treatment is often ineffective. A possible explanation for syrinx formation is fluid leakage from the microcirculation in the presence of a compromised blood-spinal cord barrier (BSCB). The aim of this study was to investigate the structural and functional integrity of the BSCB in a model of posttraumatic syringomyelia. Methods The excitotoxic amino acid and arachnoiditis model of syringomyelia was used in 27 Sprague-Dawley rats. Structural integrity of the BSCB was assessed using immunoreactivity to endothelial barrier antigen (EBA), and loss of functional integrity was assessed by extravasation of intravascular horseradish peroxidase. Animals were studied after 3 days, or at 1, 3, 6, or 12 weeks after surgery. There were laminectomy-only and saline injection control animals for comparison at each time point. Results Syrinxes formed in 16 of the 17 animals injected with excitotoxic amino acid. Loss of structural and functional integrity of the BSCB in syrinx animals was noted at all time points. Disruption of the BSCB was most dramatic in tissue adjacent to the syrinx, and in the central and dorsal gray matter. Changes in EBA expression generally corresponded with altered vascular permeability, although in the acute stages, widespread vascular permeability occurred without a corresponding decrease in EBA expression. At the later time points (3–12 weeks) EBA expression was often absent, although no vascular leakage was observed. Conclusions This study demonstrated a prolonged structural and functional disruption of the BSCB in this model of posttraumatic syringomyelia. Loss of functional integrity of the BSCB, with fluid entering the interstitial space of the spinal cord, may contribute to initial cyst formation after spinal cord injury and subsequent enlargement of the cyst, to produce posttraumatic syringomyelia.

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