Background Surgical injury induces production and release of inflammatory mediators in the vicinity of the wound. The pro-inflammatory cytokine Interleukin-1β(IL-1β) has been implicated in both inflammatory processes and nociceptive neurotransmission which plays a crucial role in this process that triggers nociceptive signaling to produce hyperalgesia and pain. Objective This article describes the biological properties of IL-1β, activation, and the possible mechanisms in postoperative pain. Content The scope of this brief review is to understand the direct and indirect roles of IL-1β in contributing to postoperative pain ,and discuss approaches to block IL-1β production or IL-1β-receptor interactions. Trend IL-1β signaling pathway plays an important role in the occurrence and development of postoperative pain. With further research, regulation of IL1-β and its signaling may be the new and effective target treatment of postoperative pain in the future.