Postherpetic neuralgia (PHN) is a complication of
herpes zoster viral infection. Its main manifestations are continuous or intermittent burning-like and electroshock-like
pain in the affected nerves.
Electroacupuncture (EA) is widely used in clinical treatment and exerts effects in alleviating
neuropathic pain. In this study, we investigated the effect and underlying mechanism of EA on PHN. Sprague-Dawley rats were treated with
resiniferatoxin (RTX) to establish a PHN model and subjected to EA and/or miR-223-3p overexpression (OV) or interference. Mechanical withdrawal latency was measured as an indication of
pain sensitivity.
Hematoxylin-
eosin staining and transmission electron microscopy were performed to observe neuron cell morphology and autophagic vacuoles, respectively. ELISA was performed to detect
reactive oxygen species (ROS) production and the levels of
tumor necrosis factor- (TNF-) α,
inducible nitric oxide synthase (iNOS),
interleukin- (IL-) 6, and
IL-10. Changes in autophagy and apoptosis-related
miRNAs were detected by immunofluorescence and qRT-PCR, respectively. In RTX-treated rats, OV and EA reduced
pain sensitivity, decreased the number of eosinophils, and increased that of nerve cells. ROS generation and the levels of TNF-α and iNOS were significantly reduced, while those of
IL-6 and
IL-10 were increased. OV and EA induced fewer autophagic vacuoles than those in the model group. The expression of
autophagy-related protein microtubule-associated protein 1 light chain 3-II, ATG9, and Rab1 was decreased by OV and EA, whereas that of P62 was increased. qRT-PCR revealed that miR-223-3p expression in the model group decreased but was increased by EA. EA inhibits neuron cell autophagy in PHN by increasing miR-223-3p expression.