Abstract: Objective: To assess the therapeutic effect of Caspase-1 inhibitor on renal injury in experimental acute pancreatitis （AP）. Methods: Forty-two SD rats were randomly divided into three groups: healthy controls （HC, n=6）; AP-S group （n=18）; AP-ICE-I group （n=18）. AP was induced by retrograde infusion of 5% sodium taurocholate into the bili-pancreatic duct in SD rats. HC rats underwent identical surgical procedures and duct cannulation without sodium taurocholate. In AP-S group, rats received the first intraperitoneal injection of isotonic saline 2 hours after induction of acute pancreatitis and repeated after 12 hours. In AP-ICE-I group, rats were firstly given ICE inhibitor intraperitoneally 2 hours after induction of pancreatitis. As in APS group, this was repeated at 12 hours. Surviving rats were killed at certain time points, and all samples were obtained for subsequent analysis. Results: The serum levels of BUN and creatinine in AP-S group were increased significantly （P＜0.01 vs HC）, which were decreased significantly at 12 h and 18 h in AP-ICE-I group （P＜0.01 vs AP-S）. The serum IL-1β levels were signi ficantly higher in AP-S group （P＜0.01 vs HC）, which were decreased significantly in AP-ICE-I group （P＜0.01 vs AP-S）. Intrarenal expressions of Caspase-1 and IL-18 mRNA could be observed, but IL-1βmRNA expression was weak in HC, which were increased significantly in AP-S group （P＜0.01 vs HC）. The expressions of IL-1β and IL-18 mRNA were decreased significantly in AP-ICE-I group （P＜0.01 vs AP-S）, whereas Caspase-1 mRNA expression had no significant differences （P＞0.05）. Caspase-1 inhibition had no effect on the severity of renal tissue damage. Conclusion: The expressions of Caspase-1 activated cytokines IL-1β and IL-18 play a pivotal role during the course of renal injury in AP. Caspase-1 inhibitor improves renal functions effectively.