AIM:Proinflammatory cytokines TNF-α and IL-6 play a mainrole in acute pancreatitis (AP).Cytokine biosynthesis runsthrough two major signaling pathways at the level ofproteins:nuclear transcription factor-κB (NF-κB) and p38mitogen-activated protein kinase (p38 MAPK).The aim ofthe study was to investigate the effect of NF-κB and p38MAPK in activated monocytes/macrophages on cytokines ofrats with acute pancreastitis.METHODS:Taurocholate (3 % and 5 %) at doses of 1 mL/kgwas administered into the biliopancreatic duct of maleSprague-Dawley (SD) rats to reduce acute edematouspancreariris (AEP) and acute necrotizing pancreatitis (ANP).Pancreatic tissues were prepared immediately after death.At this point,blood was obtained for determination of serumamylase and pro-inflammatory TNF-α and IL-6.Activatedmonocytes/macrophages were captured from blood and sowere ascites.NF-κB and p38 MAPK in activated monocytes/macrophages were measured by immunohistochemistrymethod.Pancreatic tissue samples were prepared for routinelight microscopy,using hematoxylin and eosin (HE) staining.RESULTS:The serum levels of amylase were 3 056.00±1 232.35 IU/L and 4 865.12±890.34 IU/L at 3 and 6 hoursin ANP group,which were significantly higher than those(3 056.00±1 232.35 IU/L and 3 187.17±821.16 IU/L) (P<0.05,respectively) in AEP group.In ascites the levels were3.32±1.01 g and 3.76±1.12 g at 3 and 6 hours in ANP group,which were significantly higher than those (1.43±1.02 g and2.56±1.21 g) (P<0.05,respectively) in AEP group.The serumlevels of TNF-α were 54.27±23.48 pg/ml and 67.83±22.02pg/ml in AEP group and 64.28±20.79 pg/ml and 106.59±43.71 pg/ml in ANP group,and the serum levels of IL-6 were428.12±140.30 pg/ml and 420.13±139.40 pg/ml in AEP groupand 1 600.32±309.78 pg/ml and 2 203.76±640.85 pg/ml inANP group,which were far significantly higher than those insham group (P<0.001,respectively).The serum level of TNF-α 6 hours after establishment of the studied model and thatof IL-6 at 3 and 6 hours in ANP group were significantlyhigher than those in AEP (P<0.05,P<0.001,P<0.05).InANP group,the levels of serum TNF-α and IL-6 6 hoursafter establishment of the studied model were significantlyhigher than those 3 hours after establishment of studiedmodel (P<0.05,P<0.05,respectively).Three and 6 hoursafter establishment of the model,typical pathological changes of AEP and ANP were found,such as large numbers ofinflammatory ceils,edema,hemorrhage,necrosis,largeamount of ascites.In AEP,NF-κB and p38 MAPK in activatedmonocytes/macrophages were moderately found at 3 and6 hours after introduction of the model.However,in ANP,the expression of NF-κB and p38 MAPK in activatedmonocytes/macrophages was upregulated evidently at 3 and6 hours after introduction of the model,reaching their highestlevels at 6 hours after introduction of the model,which wereconsistent with the levels of TNF-α and IL-6.CONCLUSION:Cytokine TNF-α and IL-6 play a main rolein acute pancreatitis,expression of NF-κB and p38 MAPK inactivated monocytes/macrophages might play a major rolein cytokine transcription and biosynthesis. AIM: Proinflammatory cytokines TNF-α and IL-6 play a mainrole in acute pancreatitis (AP). Cytokine biosynthesis run through two major signaling pathways at the level of proteins: Nuclear transcription factor-κB (NF-κB) and p38mitogen-activated protein kinase p38 MAPK). The aim of the study was to investigate the effect of NF-κB and p38MAPK in activated monocytes / macrophages on cytokines ofrats with acute pancreastitis. METHODS: Taurocholate (3% and 5%) at doses of 1 mL / kg was administered into the biliopancreatic duct of male Sprague-Dawley (SD) rats to reduce acute edematous pancreariris (AEP) and acute necrotizing pancreatitis (ANP). Pancreatic tissues were prepared immediately after death. At this point, blood was obtained for determination of serumamylase and pro-inflammatory TNF -α and IL-6.Activatedmonocytes / macrophages were captured from blood and sowere ascites. NF-κB and p38 MAPK in activated monocytes / macrophages were measured by immunohistochemistrymethod.Pancreatic tissue samples were prepared for routinelight microscopy, using hematoxylin and eosin (HE) staining. RESULTS: The serum levels of amylase were 3 056.00 ± 1 232.35 IU / L and 4 865.12 ± 890.34 IU / L at 3 and 6 hours in ANP group, which were both significantly higher than those (3 056.00 ± 1 232.35 IU / L and 3 187.17 ± 821.16 IU / L) (P <0.05, respectively) in AEP group. ascites the levels were 3.32 ± 1.01 g and 3.76 ± 1.12 g at 3 and 6 hours in ANP group, which were significantly higher than those (1.43 ± 1.02 g and 2.56 ± 1.21 g) (P <0.05, respectively) in AEP group. The serum levels of TNF-α were 54.27 ± 23.48 pg / ml and 67.83 ± 22.02 pg / ml in AEP group and 64.28 ± 20.79 pg / ml and 106.59 ± 43.71 pg / ml in ANP group, and the serum levels of IL-6 were 428.12 ± 140.30 pg / ml and 420.13 ± 139.40 pg / ml in AEP groupand 1 600.32 ± 309.78 pg / ml and 2 203.76 ± 640.85 pg / ml inANP group, which were far significantly higher than those insham group (P <0.001, respectively). The serum level of TNF-α 6 hours after establishment of the studied model and thatof I L-6 at 3 and 6 hours inThe ANP group were significantlyhigher than those in AEP (P <0.05, P <0.001, P <0.05) .InANP group, the levels of serum TNF-α and IL-6 6 hoursafter establishment of the studied model were significantlyhigher than those 3 hours after establishment of studied moodel (P <0.05, P <0.05, respectively). Three and 6 hours after establishment of the model, typical pathological changes of AEP and ANP were found, such as large numbers of inflamatory ceils, edema, hemorrhage, necrosis, largeamount of ascites . In AEP, NF-κB and p38 MAPK in activated monocytes / macrophages were moderately found at 3 and 6 hours after introduction of the model. However, in ANP, the expression of NF-κB and p38 MAPK in activated monocytes / macrophages was upregulated evidently at 3 and 6 hours after introduction of the model, reaching their highestlevels at 6 hours after introduction of the model, which wereconsistent with the levels of TNF-α and IL-6.CONCLUSION: Cytokine TNF-α and IL-6 play a main rolein acute pancreatitis , expression of NF-κB and p3 8 MAPK in activated monocytes / macrophages might play a major rolein cytokine transcription and biosynthesis.