Objective To investigate the mechanism of electroacupuncture (EA) intervention in the peroxisome proliferator-activated receptor-γ (PPAR-γ) pathway for improving pain in cervicalspondylotic radiculopathy (CSR) and its relationship with autophagy.

Methods Rats were divided into sham-operated group (Sham group), CSR group, EA group, EA+GW9662 (PPAR-γ antagonist) group, and EA+pioglitazone group. After 10, 20 and 30 days of intervention, the neuralgia threshold of the rats in each group was measured; the hematoxylin and eosin (HE) staining was used to observe the damage to neuronal cells in the spinal cord tissue, TUNEL was used to detect cell apoptosis, the enzyme-linked immunosorbent assay (ELISA) wasused to detect the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), prostaglandin E2 (PGE2) and β-endorphin (β-EP), and the Western blot analysis was used to detect the expression of autophagy-related proteins such as PPAR-γ, microtubule-associated protein 1 light chain 3 type Ⅱ (LC3 Ⅱ), and Beclin-1.

Results Compared with the Sham group, the CSR group showed decreased neuralgia thresholds, β-EP, PPAR-γ, LC3 Ⅱ and Beclin-1 expression levels, as well as increased cell apoptosis rate and IL-1β, IL-6, TNF-α and PGE2 levels; compared with the CSR group, the EA group, EA+GW9662 group, and EA+pioglitazone group showed increased neuralgia thresholds, β-EP, PPAR-γ, LC3 Ⅱ and Beclin-1 expression levels as well as decreased cell apoptosis rates and IL-1β, IL-6, TNF-αand PGE2 levels; the neuralgia thresholds, β-EP, PPAR-γ, LC3 Ⅱ, and Beclin-1 expression levels in the EA+GW9662 group were lower than those in the EA group, while the cell apoptosis rate and IL-1β, IL-6, TNF-α and PGE2 levels were higher; in contrast, the neuralgia thresholds, β-EP, PPAR-γ, LC3 Ⅱ and Beclin-1 expression levels in the EA+pioglitazone group were higher than those in the EA group, with lower cell apoptosis rates and IL-1β, IL-6, TNF-α and PGE2 levels; the differences mentioned above were statistically significant between the different groups (P < 0.05).

Conclusion EA inhibits pathological damage and cell apoptosis in spinal cord tissue, reduces spinal cord neuroinflammatory responses, and improves pain symptoms in CSR models by activating autophagy mediated by the PPAR-γ pathway.