Neuropathic pain is a distressing medical condition with few effective treatments, and the role of VEGFA in inflammatory pain has been confirmed in many studies. However, the mechanism by which VEGFA affects neuropathic pain remains unclear. In this study, we demonstrated that VEGFA plays an important role in spare nerve injury (SNI)-induced neuropathic pain, which is mediated by enhanced expression and colocalization of VEGFA, p-AKT and TRPV1 in an SNI-induced neuropathic pain model. Soluble VEGFR1 (sFlt1) relieved mechanical hyperalgesia and the expression of inflammatory markers and also ameliorated the expression of VEGFA, VEGFR2, p-AKT, and TRPV1 in the spinal cord. However, these effects of sFlt1 could be blocked by rpVEGFA and 740 Y-P. Therefore, our study indicates that targeting VEGFA with sFlt1 reduces neuropathic pain development via the AKT/TRPV1 pathway in SNI-induced nerve injury. This study elucidates a new therapeutic target for neuropathic pain.