objective The effect of electroacupuncture（EA） on inflammatory pain has been well recognized clinically. We previously found that EA can stimulate cannabinoid CB2 receptors in inflamed tissues. It is unclear whether CB2 receptors affect autophagy and NLRP3 inflammasome activation, contributing to the analgesic effect of EA on the inflammatory pain. Methods Inflammatory pain was induced by local injection of complete Freund’s adjuvant into the hindpaw of mice. Thermal hyperalgesia was tested with a radiant heat stimulus, and mechanical allodynia was quantified using von Frey filaments. The activation of NLRP3 inflammasome and autophagy were quantified by using Western blotting and double-immunofluorescence labeling. The number of damaged mitochondria was measured by flow cytometry.. Results Complete Freund’s adjuvant（CFA） injection activated the NLRP3 inflammasome in the skin tissue and induced pain in rats, which were attenuated by EA treatment. Increased NLRP3 inflammasomes were present in the skin macrophages, but not in T cells or keratinocytes. CFA reduced autophagy in the inflamed skin tissues, which was largely reversed by EA treatment. In CB2 receptor-knockout mice, the analgesic effect of EA and its effects on NLRP3 inflammasomes and autophagy were largely attenuated. In addition, in a macrophage cell line, CB2 receptor stimulation inhibited the NLRP3 inflammasome activation by promoting autophagy and reducing the number of damaged mitochondria. Conclusions Our results suggest a novel signaling pathway through which CB2 receptors are involved in the analgesic effect of EA on inflammatory pain. Stimulation of CB2 receptors promotes autophagy to inhibit NLRP3 inflammasome activation in inflamed skin tissues.