脓毒症引发急性肾损伤(acute kidney injury，AKI)的过程中，炎症因子发挥了重要作用。P 物质(substance P，SP)具有很强的促炎作用。研究发现脓毒症患者血清中SP 明显高于对照组。并有研究发现SP 通过增强氧化应激和巨噬细胞浸润促进肾损伤，NK1 受体(NK1 receptor,NK1R)抑制剂能阻止以上肾损伤。推测SP 在脓毒症引发AKI 的过程中，通过招募和激活中性粒细胞，促进炎症反应和活性氧(reactive oxygen species，ROS)的产生；通过调控不同类型的巨噬细胞，促进炎症、ROS 生成，增加免疫抑制；促进肾小管细胞凋亡。

Inflammatory factors play an important role in sepsis-induced AKI. Substance P (SP) level is elevated significantly in sepsis patients as compared with that in the control group. Higher SP level contributes to renal damage possibly via enhancing oxidative stress and macrophage infiltration to the kidney, and NK1 receptor antagonists alleviate the renal injury. It is suggested that SP promotes inflammation, ROS production and immunosuppression through the recruitment of leukocytes and the regulation of different types of macrophages.