Abstract： The purpose of this study was to investigate whether activation of TRPA1 is involved in the formation of crush injury induced neuropathic pain and its mechanism. At 2 h and 4 h after administration of TRPA1 inhibitor, mice models presented significantly longer paw withdrawal thermal latency and lower cold pain ratings compared with those without intervention ( P<0.05) . Compared with those without intervention, the levels of TRPA1 protein in brain tissue of mice model were significantly lower at 2 h and 4 h of administration, with statistically significant difference ( P<0.05) . In summary, activation of TRPA1 plays an important role in regulation and transmission of neuropathic pain induced by crush injury.