Mechanism of Electroacupuncture at Jiaji Acupoints (EX‐B2) Improving Neuropathic Pain in Cervical Spondylotic Radiculopathy Rats via Modulating Microglial STAT3 Phosphorylation and Mitochondrial Function

Neuropathic pain in cervical spondylotic radiculopathy (CSR) remains a therapeutic challenge, with mounting evidence implicating microglia‐driven neuroinflammation as a key contributor. Here, we demonstrate that electroacupuncture (EA) at Jiaji (EX‐B2) acupoints relieves CSR‐induced neuropathic pain by targeting microglial signal transducer and activator of Transcription 3 (STAT3) signaling. In a CSR rat model, EA significantly improved sensorimotor outcomes. EA suppressed STAT3 phosphorylation in dorsal horn microglia, accompanied by reduced expression of proinflammatory cytokines (TNF‐ α and IL‐6) and reactive oxygen species (ROS). In vitro, serum from EA‐treated rats replicated these anti‐inflammatory effects in lipopolysaccharide (LPS)–activated BV‐2 microglial cells. Mechanistically, EA inhibited microglial STAT3 activation and upregulated the mitochondrial complex I subunit NDUFA13, restoring mitochondrial membrane potential and limiting oxidative stress. Furthermore, EA reversed CSR‐induced imbalances in spinal nociceptive (CGRP) and axonal structural (NF200) markers, promoting a homeostatic microenvironment. Together, these findings identify microglial STAT3 as a critical target of EA and reveal a “STAT3–mitochondrial axis” underlying its analgesic effect. Our study provides a mechanistic rationale for applying Jiaji acupoints EA in CSR‐induced neuropathic pain and potentially other neuroinflammatory disorders.