OBJECTIVE: To explore the effect of the activated NF-kappaB and the interaction between activated NF-kappaB and tumor necrosis factor (TNF)-alpha in the process of acute pancreatitis. METHODS: 64 Wistar rats were randomly divided into two groups of 32 rats: pancreatitis group (to be made pancreatitis models) and control group. 1.5, 3.0, 6.0, and 12.0 hours after the onset of experiment the amount of ascitic fluid was measured, blood was extracted from abdominal aorta, changes of pancreas was observed, pancreatic tissues were stained with HE, and flow cytometry (FCM) and enzyme linked immuno-sorbent assay (ELISA) were used to examine the content of TNF-alpha protein and activation of NF-kappaB (number of positive cells/50 micro l) in the pancreatic tissues. The contents of amylase and lipase in plasma were examined. The pathology of pancreatic tissue was graded. RESULTS: The levels of activated NF-kappaB and TNF-alpha protein in the pancreatic tissue were all significantly higher than those of the control group at any time point (all P < 0.05). The levels of activation of NF-kappaB of the pancreatitis group at any time point were significantly higher than those of the control group (all P < 0.01) and reached its maximum about 3.0 hours after the onset of experiment and then declined. The levels of plasma amylase and lipase were significantly higher in the pancreatic group than in the control group at any rime point. (all P < 0.01). In the pancreatic group severe edema and congestion were found at the 3.0 h time point and bleeding and necrosis were found at the 6.0-hour time point. CONCLUSION: Activated NF-kappaB as initial factor plays an important role in the pathogenesis of acute pancreatitis, activates a lot of inflammatory media, and induces cascading reaction of inflammation. TNF-alpha is a pivotal factor in pancreatitis pathogenesis, it cooperates with amylase and lipase to intensify the leisure in pancreatic tissue resulting bleeding and necrosis.
OBJECTIVE: To explore the effect of the activated NF-kappaB and the interaction between activated NF-kappaB and tumor necrosis factor (TNF)-alpha in the process of acute pancreatitis. METHODS: 64 Wistar rats were randomly divided into two groups of 32 rats: pancreatitis group (to be made pancreatitis models) and control group. 1.5, 3.0, 6.0, and 12.0 hours after the onset of experiment the amount of ascitic fluid was measured, blood was extracted from abdominal aorta, changes of pancreas was observed, pancreatic tissues were stained with HE, and flow cytometry (FCM) and enzyme linked immuno-sorbent assay (ELISA) were used to examine the content of TNF-alpha protein and activation of NF-kappaB (number of positive cells/50 micro l) in the pancreatic tissues. The contents of amylase and lipase in plasma were examined. The pathology of pancreatic tissue was graded. RESULTS: The levels of activated NF-kappaB and TNF-alpha protein in the pancreatic tissue were all significantly higher than those of the control group at any time point (all P < 0.05). The levels of activation of NF-kappaB of the pancreatitis group at any time point were significantly higher than those of the control group (all P < 0.01) and reached its maximum about 3.0 hours after the onset of experiment and then declined. The levels of plasma amylase and lipase were significantly higher in the pancreatic group than in the control group at any rime point. (all P < 0.01). In the pancreatic group severe edema and congestion were found at the 3.0 h time point and bleeding and necrosis were found at the 6.0-hour time point. CONCLUSION: Activated NF-kappaB as initial factor plays an important role in the pathogenesis of acute pancreatitis, activates a lot of inflammatory media, and induces cascading reaction of inflammation. TNF-alpha is a pivotal factor in pancreatitis pathogenesis, it cooperates with amylase and lipase to intensify the leisure in pancreatic tissue resulting bleeding and necrosis.