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Gua Sha Alleviates Radiculitis-Induced Pain Via HIF-1α-Mediated Metabolic Reprogramming Pathway in Rats
Haotian Ge1, Shuxia Yan1, Mingwan Yin1
1School of Nursing, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.
Pain Research & Management
|March 25, 2025
Summary
Gua Sha therapy alleviates radiculitis-induced pain by improving blood flow and reducing inflammation. This involves inhibiting hypoxia-inducible factor 1-alpha (HIF-1α)-mediated metabolic changes in the dorsal root ganglion.
Area of Science:
- Neuroscience
- Pain Management
- Metabolic Regulation
Background:
- Radiculitis-induced pain (RIP) stems from dorsal root ganglion (DRG) inflammation and sensitization.
- The role of hypoxia-inducible factor 1-alpha (HIF-1α) in RIP pathogenesis and the therapeutic mechanisms of Gua Sha remain unclear.
- Gua Sha therapy has demonstrated potential in reducing inflammation and neural damage associated with lumbar disc herniation (LDH).
Purpose of the Study:
- To investigate the role of HIF-1α-mediated metabolic reprogramming in RIP.
- To determine if Gua Sha therapy alleviates RIP by targeting HIF-1α-driven metabolic pathways.
- To elucidate the underlying mechanisms of Gua Sha's pain-relieving effects in RIP.
Main Methods:
- Male Sprague-Dawley rats underwent LDH surgery and were assigned to sham, model, or Gua Sha treatment groups (including with DMOG or YC-1).
- Gua Sha therapy was administered over three courses post-surgery.
- Pain behaviors (paw withdrawal threshold/latency), DRG/serum inflammatory markers (IL-1β, TNF-α, NF-κB), microcirculation, DRG hypoxia, and expression of HIF-1α and related metabolic factors (GLUT1, PFKM, PDK1) were assessed.
Main Results:
- Gua Sha treatment significantly improved pain scores and reduced inflammatory markers in serum and DRG tissue.
- Gua Sha enhanced microcirculation, alleviated DRG hypoxia, and decreased levels of HIF-1α, lactic acid, and related metabolic reprogramming factors, while increasing ATP levels.
- DMOG (HIF-1α activator) reversed Gua Sha's beneficial effects, whereas YC-1 (HIF-1α inhibitor) showed effects comparable to Gua Sha alone.
Conclusions:
- HIF-1α-mediated metabolic reprogramming is a key mechanism contributing to RIP.
- Gua Sha therapy effectively alleviates RIP by improving DRG microcirculation and oxygenation, thereby inhibiting HIF-1α-driven metabolic reprogramming and reducing DRG sensitization and inflammation.
- This study highlights Gua Sha as a potential therapeutic intervention for RIP by targeting metabolic pathways involved in neuroinflammation.
