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Diabetic neuropathic pain (DNP) is a common complication of diabetes, and its complicated pathogenesis as well as clinical manifestations has brought great troubles to clinical treatment. The spinal cord is an important part of regulating the occurrence and development of DNP. Spinal microglia can regulate the activity of spinal cord neurons and have a regulatory effect on chronic pain. P2Y12 receptor is involved in DNP. P2Y14 and P2Y12 receptor belong to the Gi subtype of P2Y receptors, but there is no report that P2Y14 receptor is involved in DNP. Closely related to many human diseases, the dysregulation of lncRNA has the effect of promoting or inhibiting the occurrence and development of diseases. The aim of this research is to investigate the function of spinal cord P2Y14 receptor in type 2 DNP and to understand the function as well as the possible mechanism of lncRNA-UC.25+ (UC.25+) in rat spinal cord P2Y14 receptor-mediated DNP. Our results showed that P2Y14 shRNA can reduce the expression of P2Y14 in DNP rats, thereby restraining the activation of microglia, decreasing the expression of inflammatory factors and the level of p38 MAPK phosphorylation. At the same time, UC.25+ shRNA can down-regulate the expression of P2Y14 receptor, reduce the release of inflammatory factors, and diminish the p38 MAPK phosphorylation, indicating that UC.25+ can alleviate spinal cord P2Y14 receptor-mediated DNP. The RNA immunoprecipitation result showed that UC.25+ enriched STAT1 and positively regulated its expression. The chromatin immunoprecipitation result indicated that STAT1 combined to the promoter region of P2Y14 receptor and positively regulated the expression of P2Y14 receptor. Therefore, we infer that UC.25+ may alleviate DNP in rats by regulating the expression of P2Y14 receptor in spinal microglia via STAT1.