Reactive oxygen species (ROS) play a critical role in the pathogenesis of neuropathic pain, but few studies have examined the role of oxidative stress in the mirror-image neuropathic pain (MINP). The present study was to investigate the role of ROS in MINP caused by chronic compression of the dorsal root ganglion (DRG) (CCD) in a rat model. SD rats were randomly divided into sham group and CCD group. CCD was conducted to induce MINP. CCD rats were intraperitoneally injected with α-Phenyl-N-tert-butyl-nitrone (PBN) at 7 days after surgery. Paw withdrawal mechanical threshold (PWMT) was measured at -1, 1, 3, 5 and 7 days after surgery in sham group and CCD group, and at 8 time points after PBN injection. Rats were sacrificed at 3 and 7 days after surgery in sham group and CCD group and at 0.5 and 2 h after PBN injection, and the superoxide dismutase (SOD) and catalase activities, as well as hydrogen peroxide (H2O2) and malonaldehyde (MDA) contents were determined in the contralateral DRGs. Results showed bilateral PWMT reduced significantly in sham group and CCD group, but it returned to nearly normal level in sham group. MDA content, H2O2 content and SOD activity increased significantly, while catalase activity remained unchanged in CCD rats. PBN at 100 mg/kg significantly attenuated bilateral mechanical hyperalgesia accompanied by the improvement of oxidative stress in the contralateral DRGs. Our results demonstrate that ROS produced in the contralateral DRG are involved in the pathogenesis of CCD induced MINP, and ROS scavenger may be a promising drug for the therapy of MINP.
Keywords: Mechanical hyperalgesia; Mirror-image neuropathic pain; Oxidative stress; Phenyl-N-tert-butylnitrone; Reactive oxygen species.