Abstract
BackgroundCervical spondylotic myelopathy (CSM) is a spinal cord disease caused by cervical disc degeneration and related pathological changes. Cervical spondylotic myelopathy may result from inflammation responses and neuronal damage. Thioredoxin-interacting protein (TXNIP)/NOD-like receptor protein 3 (NLRP3) signaling promotes inflammation. However, the effects of TXNIP/NLRP3 on the pathogenesis of CSM have not been reported.MethodsA rat model of chronic cervical cord compression was established to observe changes in the levels of of TNXIP/NeuN and NLRP3/NeuN expression in the damaged anterior horn of the spinal cord following progression of CSM. Rats were injected with TXNIP small interfering RNA (siRNA) and scrambled control to determine the effects of TXNIP inhibition on NLRP3-mediated inflammation in rats with CSM. Behaviors effects and the expression of NLRP3 and pro-caspase-1 in the damaged spinal cord were evaluated.ResultsThe expression levels of TXNIP and NLRP3 were significantly increased in the damaged anterior horn of the spinal cord following CSM. Injection of TXNIP siRNA significantly improved behavioral measures and decreased apoptosis in the damaged anterior horn of spinal cord. Furthermore, the levels of NLRP3 and pro-caspase-1 in the lesioned area were reduced by the TXNIP siRNA injection.ConclusionThioredoxin-interacting protein participated in NLRP3 mediated inflammation in a rat model of CSM, which indicated that TXNIP may be a potential therapeutic target in improving CSM.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.