Electroacupuncture regulates microglia activation through theSTING/NF-κB pathway to reduce pain in bone cancer pain mouse

Cancer pain is a global public health problem. The mechanism of cancer pain is complex, and opioid analgesics, which are widely used clinically, have obvious addiction and side effects, which seriously affect patientslife functions and may aggravate their anxiety, depression and other negative emotions. Acupuncture has a history of thousands of years in China, and acupuncture analgesia has been confirmed by many studies. This study investigated whether electroacupuncture can alleviate abnormal pain in bone cancer pain (BCP) mouse models and its possible central mechanism. A bone cancer pain model was established by injecting Lewis lung cancer cells into the left femoral cavity of adult male mice. Mechanical paw withdrawal threshold was tested baseline before surgery and 1, 4, 7, 10, 14 and 21 days after surgery. On day 21, behaviours related to depression emotions were tested. After the behaviours, the femurs were removed to observe pathological changes, the neck was broken and brain tissue was collected from the basal lateral amygdala (BLA) area for subsequent Western Blot and ELISA experiments were performed to verify the expression of (stimulator of interferon genes, STING) STING/NF-{kappa}B pathway proteins and the expression of inflammatory factors. Immunofluorescence of Ionized calcium-binding adapter molecule-1 (Iba-1) and STING in the basal lateral amygdala (BLA) brain region was also performed. The results show that electroacupuncture can increase the pain threshold of the bone cancer pain model and alleviate the depressive-like emotional phenotype. Electroacupuncture inhibited the expression of STING/NF-{kappa}B pathway proteins, activation of microglia and release of inflammatory factors in the basal lateral amygdala (BLA) area. Therefore, this study shows that electroacupuncture may relieve bone cancer pain by regulating microglial activation and inflammatory factor release through the STING/NF-{kappa}B pathway.