Fire Acupuncture Combined with Pulse Radiofrequency Relieves Tactile Allodynia in Rats with Postherpetic Neuralgia.

Postherpetic neuralgia (PHN) remains challenging to treat, with 40%-50% of patients experiencing inadequate pain relief despite comprehensive interventions. Neuromodulation techniques such as pulsed radiofrequency (RF) and traditional methods such as fire acupuncture (FA) are increasingly used for PHN. This study investigated the combined effect of FA and RF on tactile allodynia in a rat model of PHN and explored its underlying mechanisms. Adult male rats were randomly divided into: Control, PHN, FA, RF, and combined FA_RF groups. PHN was induced by varicella-zoster virus inoculation. FA and/or RF interventions began on Day 15. Pain behavior was assessed via mechanical allodynia and thermal hyperalgesia tests. On Day 37, spinal cord tissues and cerebrospinal fluid were collected to evaluate astrocyte and microglial activation, neuronal apoptosis, expression of Insulin-Like Growth Factor 2 (IGF2), Peripheral Myelin Protein 2 (PMP2), Claudin-19 (CLDN19), Homeobox C8 (HOXC8), and levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor-α (TNF-α). The role of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway was verified using a PI3K/AKT agonist. The results revealed that mechanical allodynia thresholds decreased on Day 8 post-inoculation. Compared to the PHN group, FA_RF combination significantly increased mechanical thresholds and prolonged thermal hyperalgesia latency, with superior effects versus FA or RF alone. The FA_RF group showed increased spinal IGF2, PMP2, and CLDN19 expression, decreased HOXC8, reduced astrocyte activation, and modulated cytokine levels (IL-1β, IL-6, TNF-α, IL-10). The PI3K/AKT agonist reversed the analgesic effects of FA_RF. Combined fire acupuncture and pulsed radiofrequency alleviates tactile allodynia in PHN rats, possibly by inhibiting spinal astrocyte activation, modulating inflammatory responses, and promoting nerve repair via IGF2, PMP2, and CLDN19 expression. The PI3K/AKT pathway may be critically involved in this analgesic mechanism.