Objective To investigate the analgesic effect of repetitive transcranial magnetic stimulation (rTMS) on rats with neuropathic pain (NPP) caused by chronic compression of dorsal root ganglion (CCD) and to explore the mechanism. Methods A total of 36 male rats aged 10 weeks were evenly randomized into 3 groups:sham operation+sham stimulation group, NPP+sham stimulation group, and NPP+rTMS group. The rats in the sham operation+sham stimulation group and NPP+sham stimulation group received sham stimulation in the morning and afternoon, while the rats in the NPP+rTMS group received sham stimulation in the morning and high frequency rTMS (M1 area of cerebral cortex, 20 Hz) in the afternoon. On the 8^th day after CCD-caused NPP modeling, rats were intervened by rTMS or sham stimulation for 11 consecutive days. Von Frey filaments and conditioned place preference test were used to evaluate the mechanical withdrawal threshold and spontaneous pain before and after rTMS intervention. The left L₄-L₅ dorsal root ganglion (DRG), spinal cord dorsal horn and sera were collected on the 20^th day after NPP modeling, the expression levels of glial fibrillary acidic protein (GFAP), an activation marker of satellite glial cells and astrocytes, in DRG and spinal cord dorsal horn and the postsynaptic density-95 (PSD-95) in spinal cord dorsal horn were measured by Western blotting. The interleukin 18 (IL-18) and tumor necrosis factor α (TNF-α) in sera were detected by enzyme-linked immunosorbent assay (ELISA). Results Compared with the sham operation+sham stimulation group, the mechanical withdrawal threshold was significantly decreased, the expression of GFAP in DRG was significantly increased, the expression levels of GFAP and PSD-95 in spinal cord dorsal horn were significantly higher, and the serum levels of IL-18 and TNF-α were significantly increased in the NPP+sham stimulation group (all P<0.05); and the rats in the 2 groups had no preference for cage A or cage B. However, these changes were all reversed in the NPP+rTMS group after receiving high-frequency rTMS, and the rats had a preference for cage B compared with the NPP+sham stimulation group (all P<0.05). Conclusion High-frequency rTMS may relieve CCD-caused NPP by inhibiting the activation of satellite glial cells in DRG, by inhibiting astrocyte activation and synaptic connection formation in spinal cord dorsal horn, and by improving inflammatory microenvironment.