Effects of stellate ganglion block on inflammation and autophagy of spinal cord neurons in rats with neuropathic pain after spinal cord injury

Objective: To assess the therapeutic effects of stellate ganglion block (SGB) on spinal cord injury (SCI)- induced neuropathic pain in rats, and to explore its potential mechanisms in alleviating neuropathic pain, thereby providing a theoretical foundation for clinical treatment. Methods: A rat model of SCI was established, and animals were randomly assigned to one of three groups: the sham surgery group (Sham), the SCI group (SCI), or the SCI group treated with SGB (SCI + SGB). Motor function was assessed using the Basso Beattie Bresnahan (BBB) loco-motor rating scale, while thermal hyperalgesia was evaluated using hot plate test. Enzyme-linked immunosorbent assay (ELISA) was utilized to measure the levels of inflammatory cytokines, including interleukin-1(3 (IL-1(3), IL-6, and tumor necrosis factor-alpha (TNF-alpha), within the spinal cord. Hematoxylin-eosin (HE) staining was performed to observe spinal cord histopathology. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining was used to detect apoptotic cells, and transmission electron microscopy was employed to visualize autophagosomes. Expression of autophagy-related proteins LC3-II/LC3-I and p62 was examined via Western blotting. Results: Compared with the sham group, rats in the SCI group displayed impaired hind limb motor function, decreased pain thresholds, elevated inflammatory cytokine levels, significant spinal cord pathology, increased apoptosis, altered expression of autophagy-related protein, and disrupted autophagic flux. In contrast, SGB treatment improved motor function, alleviated pain, reduced inflammatory cytokines levels, mitigated spinal cord injury and apoptosis, and enhanced autophagy with improved autophagic flux. Conclusions: Stellate ganglion block alleviates neuropathic pain in SCI-induced rats by reducing pro-inflammatory cytokine levels, mitigating spinal cord apoptosis and injury, promoting autophagy, and restoring autophagic flux in the spinal cord.