Gua Sha Alleviates Radiculitis‐Induced Pain Via HIF‐1α–Mediated Metabolic Reprogramming Pathway in Rats

<b>Background:</b> Radiculitis-induced pain (RIP) results from dorsal root ganglion (DRG) sensitization due to inflammation. Hypoxia-inducible factor 1-alpha (HIF-1<i>α</i>) is linked to inflammatory responses through metabolic changes, but its role in RIP is not well understood. Gua Sha therapy has been shown to reduce inflammation and neural damage from lumbar disc herniation (LDH). This study investigates whether HIF-1α-mediated metabolic reprogramming contributes to the pain-relieving effects of Gua Sha in RIP. <b>Methods:</b> Male SD rats were subjected to LDH surgery and divided into six groups: sham, model, sham Gua Sha, Gua Sha, Gua Sha + DMOG, and Gua Sha + YC-1. Gua Sha was applied 5 days postsurgery, every other day for three sessions per course, totaling three courses. Changes in paw withdrawal threshold (PWT) and latency (PWL) were monitored, along with blood flow in the rats' backs. Levels of IL-1β, TNF-<i>α</i>, and NF-κB were assessed in serum and DRG tissue. Pathological changes and hypoxia in DRG tissues were observed using hematoxylin-eosin staining and immunofluorescence. Western blotting and qPCR measured HIF-1α, GLUT1, PFKM, and PDK1 expression, while lactic acid and ATP levels in DRG tissue were also evaluated. <b>Results:</b> Gua Sha increased PWT and PWL, reduced serum and DRG inflammatory factors, improved back microcirculation, alleviated DRG hypoxia, and decreased HIF-1α and related signaling factors. It also lowered lactic acid and raised ATP levels. DMOG, a HIF-1α activator, reversed these effects. HIF-1α activation did not affect serum inflammatory factors but partially improved PWT. Inhibition of HIF-1α with YC-1 did not significantly differ from Gua Sha alone. <b>Conclusion:</b> HIF-1α-mediated metabolic reprogramming is a pathogenic mechanism in RIP. Gua Sha alleviates RIP by enhancing microcirculation, improving DRG hypoxia, inhibiting HIF-1α-mediated reprogramming, and reducing DRG sensitization and inflammation. This study provides insights into the mechanisms of Gua Sha's therapeutic effects in RIP.