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Early high-frequency spinal cord stimulation modulates the ROS/p38 MAPK/NF-κB and CXCL10/CXCR3 pathways to alleviate neuropathic pain and promote spinal cord injury repair

ABSTRACT: High-frequency spinal cord stimulation (HF-SCS) has been proven to be an effective method for treating neuropathic pain, but its specific mechanism of action in spinal cord injury (SCI) remains unclear. This study aims to explore the therapeutic effect of early HF-SCS in a rat model of SCI and its potential molecular mechanism. The SD rat model of T10 spinal cord contusion was established, and stimulation electrodes were implanted epidurally, followed by HF-SCS treatment (movement threshold 40%, frequency 10,000 Hz). The results showed that HF-SCS significantly attenuated SCI-induced neuropathic pain, facilitated functional recovery, and accelerated axonal regeneration and myelin repair. Further mechanism studies indicated that HF-SCS exerts its neuroprotective effect by down-regulating the ROS/p38 MAPK/NF-κB signaling pathway to reduce microglial activation and decrease the release of pro-inflammatory factors; simultaneously, it inhibits the activation of the CXCL10/CXCR3 axis to alleviate central sensitization. This study suggests that early HF-SCS intervention can improve the functional prognosis after SCI by suppressing neuroinflammation and reducing central sensitization, thereby providing a theoretical basis for the treatment of SCI with HF-SCS.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE332999 | GEO | 2026/07/14

REPOSITORIES: GEO

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Project description:Objective: Chronic pain is a major problem in patients with spinal cord injury (SCI). According to different studies, approximately 70% of patients with SCI experience persistent pain. Although previous gene expression profiling studies have been conducted in animal models, gene expression profiling study in human whole blood has not been reported yet. The objective of this study was to define the gene expression profile of neuropathic pain in spinal cord injured patients. Materials and Methods: We performed gene expression analysis including 20.000 genes using Affymetrix GeneChip® Primeview™ Human Gene Expression Arrays. For confirmation of expression levels of selected genes, we performed real time polymerase chain reaction. We gathered samples from periferic blood mononuclear cells. Data of twelve patients with intractable neuropathic pain was compared with thirteen patients who don’t have pain. All patients have complete injuries with a level of injury above T5. Results: A total of 16 differentially expressed genes including 9 up-regulated and 7 down-regulated were obtained with a cut-off degree at 4 fold change. EIF1AY, RPS4Y1, DDX3Y, RPL31, ETS1, KLF3, JUN, CYorf15B, and ERAP2 were in up-regulated and HLA-C, XIST, C4BPA, FAM118A, ZNF506, OVOS2, and C1D were in down-regulated group. KEGG pathway database showed that 14.6% of genes were enriched in the nodes of immune system. Real time polymerase chain reaction analyses did not increase to statistically significant levels for confirmation of gene expression analyze results. Conclusions: Considering these data, findings of this first gene expression study in humans with SCI might provide valuable information for future targets for understanding neuropathic pain pathogenesis. The results of gene expression analyses were not confirmed by real time polymerase chain reaction. Studies with larger sample size are needed for confirmation. This is a cross-sectional study with a control group. Patients were divided into two groups according to intractable neuropathic pain existence.There were 12 patients in group A (Patients with pain) and 13 patients in control group.

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Early high-frequency spinal cord stimulation modulates the ROS/p38 MAPK/NF-κB and CXCL10/CXCR3 pathways to alleviate neuropathic pain and promote spinal cord injury repair

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