AIM: To investigate the effect of selective Cycloo- xygenase-2 (COX-2) inhibitor 4-[5-(4-Chloro-phenyl)-3- (trifluoromethyl)-1H-pyrazol-1-yl] benzenesulfonamide (SC-236), on the cholecystokinin (CCK)-octapeptide- induced acute pancreatitis (AP) in rats. METHODS: Wistar rat weighing 240 g to 260 g were divided into three groups. (1) Normal DMSO treated group, (2) SC-236 at 4 mg/kg treated group; SC-236 systemically administered via the intravenous (i.v.) catheter, followed by 75 μg/kg CCK octapeptide subcutaneously three times, after 1, 3 and 5 h. This whole procedure was repeated for 5 d. (3) Dimethyl sulfoxide (DMSO) treated group: an identical protocol was used in this group as in the SC-236 cohort (see 2. above). Repeated CCK octapeptide treatment resulted in a typical experimentally induced pancreatitis in the Wistar rats. RESULTS: SC-236 improved the severity of CCK- octapeptide-induced AP as measured by laboratory criteria [the pancreatic weight/body weight (p.w/ b.w) ratio, the level of serum amylase and lipase]. The SC-236 treated group showed minimal histologic evidence of pancreatitis and a significant reduction inmyeloperoxidase activity. SC-236 also increased heat shock protein (HSP)-60 and HSP72 compared with the DMSO-treated group in the CCK-octapeptide-induced AP and also reduced the pancreatic levels of COX-2. Furthermore, SC-236 reduced proinflammatory cytokine synthesis and inhibited NF-κB activation compared with the DMSO-treated group in the CCK-octapeptide-induced AP. CONCLUSION: Our results suggested that COX-2 plays pivotal role in the development of AP and COX-2 inhibitors may play a beneficial role in preventing AP. AIM: To investigate the effect of selective cyclo-xygenase-2 (COX-2) inhibitor 4- [5- (4-Chloro- phenyl) -3- METHODS: Wistar rat weighing 240 g to 260 g was divided into three groups. (1) Normal DMSO treated group, (2) SC- 236 at 4 mg / kg treated group; SC-236 systemically administered via the intravenous (iv) catheter, followed by 75 μg / kg CCK octapeptide subcutaneously three times, after 1, 3 and 5 h. (3) Dimethyl sulfoxide (DMSO) treated group: an identical protocol was used in this group as in the SC-236 cohort (see 2. above). Repeated CCK octapeptide treatment resulted in a typical experimentally induced pancreatitis in the Wistar rats. RESULTS: SC-236 improved the severity of CCK-octapeptide-induced AP as measured by laboratory criteria [the pancreatic weight / body weight (pw / bw) ratio, the level of serum amylase and lipase]. The SC-236 treated group showed minimal histologic evidence of pancreatitis and a significant reduction in myeloperoxidase activity. SC-236 also increased heat shock protein (HSP) -60 and HSP72 compared with the DMSO-treated group in the CCK-octapeptide-induced AP and also reduced the pancreatic levels of COX-2. Furthermore, SC-236 reduced proinflammatory cytokine synthesis and inhibited NF-κB activation compared with the DMSO-treated group in the CCK-octapeptide-induced AP. CONCLUSION : Our results suggested that COX-2 plays a pivotal role in the development of AP and COX-2 inhibitors may play a beneficial role in preventing AP.