5th Edition of International Neurology Conference 2026

Abstract

Neuropathic pain is a debilitating chronic pain condition caused by lesions or diseases of the somatosensory nervous system and is characterized by persistent mechanical allodynia, thermal hyperalgesia, and spontaneous pain. Accumulating evidence indicates that satellite glial cells (SGCs) surrounding primary sensory neurons in the dorsal root ganglia (DRG) play a critical role in the initiation and maintenance of peripheral sensitization following nerve injury. However, the upstream regulatory mechanisms governing SGC inflammatory activation remain incompletely understood. MicroRNA-9 (miR-9), a highly conserved microRNA enriched in the nervous system, has emerged as an important post-transcriptional regulator of neuroinflammation and neuronal plasticity. The present study investigated whether miR-9 alleviates neuropathic pain by suppressing inflammatory activation of DRG SGCs and subsequently attenuating neuronal sensitization.

A neuropathic pain model was established using peripheral nerve injury, and pain-related behavioral responses were assessed by measuring mechanical withdrawal thresholds and thermal withdrawal latencies. The expression of miR-9 and markers associated with SGC activation and inflammatory responses in the DRG was evaluated using quantitative real-time polymerase chain reaction, Western blotting, immunofluorescence staining, and related molecular biological approaches. Primary DRG-derived SGCs were further cultured and stimulated under inflammatory conditions to investigate the direct regulatory effects of miR-9 on glial activation. In addition, SGC–DRG neuron co-culture systems were employed to determine whether changes in SGC inflammatory status affected neuronal activation and sensitization.

Peripheral nerve injury induced pronounced SGC activation in the DRG, as evidenced by increased expression of glial fibrillary acidic protein (GFAP), accompanied by enhanced production of pro-inflammatory mediators, including tumor necrosis factor-α, interleukin-1β, and interleukin-6. These alterations were associated with increased activation of adjacent sensory neurons and the development of persistent pain hypersensitivity. Notably, miR-9 expression was altered during the development of neuropathic pain, suggesting its potential involvement in the regulation of the DRG inflammatory microenvironment. Restoration or overexpression of miR-9 markedly suppressed SGC activation, reduced the expression and release of pro-inflammatory cytokines, and attenuated inflammation-related intracellular signaling. Moreover, miR-9-mediated inhibition of SGC inflammatory activation significantly reduced neuronal hyperexcitability and decreased the expression of neuronal activation markers in SGC–neuron co-culture systems. Consistent with these cellular findings, enhancement of miR-9 signaling in vivo ameliorated nerve injury-induced mechanical allodynia and thermal hyperalgesia.

Collectively, these findings suggest that miR-9 functions as an endogenous negative regulator of SGC-mediated neuroinflammation in the DRG. By suppressing the inflammatory activation of SGCs and disrupting pathological glia–neuron communication, miR-9 limits peripheral neuronal sensitization and alleviates neuropathic pain. Targeting the miR-9-mediated regulatory network within DRG SGCs may therefore represent a promising therapeutic strategy for the treatment of neuropathic pain.