摘要
Objective: To explore the characteristics of NF-闎 activation in the progress of pancreatitis, the relationship with expression of TNF- in the inflammatory reaction, and prevent the exacerbation of pancreatitis by using NAC. Method: Forty-eight rats were divided into three groups: therapy (group C), pancreatitis (group B) and control (group A). NAC served as the inhibitor of NF-闎 activation. In the time intervals of 1.5, 3.0, 6.0, 12.0 hour, NF-闎 activation was detected with flow cytometry (FCM) and the expression of TNF- mRNA and protein with in situ hybridization (ISH) and enzyme-linked immuno-sorbent assay (ELISA) respectively. Meanwhile, the level of lipase and amylase in the serum was assayed and the pathological change was evaluated. Result: NF-闎 activation in the pancreatitis group was higher than that in the control group (P<0.01), peaked at 3 hours, and was depressed by the inhibitor of NF-闎, NAC. The expression of TNF- as well as the level of lipase and amylase in the serum also rose synchronously with activation of NF-闎. In contrast to group A, it was significantly different (P<0.01) in group B. After using NAC in group C, all of these values were decreased and the in-flammatory reaction in the pancreas abated evidently. The pathology changes of the pancreas were shown to be alleviated in group C. Conclusion: First, NF-闎 activity is intensively initiated in the course of pancreatitis and shown to have closely relationship with the release of cytokines. Second, use of NAC markedly depressed NF-闎 activation. TNF- expression is down regulated by cytokines. It is suggested that NAC probably acts as a useful agent for treatment of pancreatitis by indirectly inhibiting activation of NF-闎.
Objective:To explore the characteristics of NF-κB activation in the progress of pancreatitis，the relationship with expression of TNF-α in the inflammatory reaction, and prevent the exacerbation of pancreatitis by using NAC.Method:Forty-eight rats were divided into three groups: therapy (group C), pancreatitis (group B) and control (group A).NAC served as the inhibitor of NF-κB activation.In the time intervals of 1.5, 3.0, 6.0, 12.0 hour, NF-κB activation was detected with flow cytometry (FCM) and the expression of TNF-α mRNA and protein with in situ hybridization (ISH) and enzyme-linked immuno-sorbent assay (ELISA) respectively. Meanwhile, the level of lipase and amylase in the serum was assayed and the pathological change was evaluated. Result:NF-κB activation in the pancreatitis group was higher than that in the control group (P<0.01),peaked at 3 hours,and was depressed by the inhibitor of NF-κB, NAC.The expression of TNF-α as well as the level of lipase and amylase in the serum also rose synchronously with activation of NF-κB.In contrast to group A, it was significantly different (P<0.01) in group B.After using NAC in group C,all of these values were decreased and the inflammatory reaction in the pancreas abated evidently. The pathology changes of the pancreas were shown to be alleviated in group C. Conclusion: First,NF-κB activity is intensively initiated in the course of pancreatitis and shown to have closely relationship with the release of cytokines. Second, use of NAC markedly depressed NF-κB activation. TNF-α expression is down regulated by cytokines. It is suggested that NAC probably acts as a useful agent for treatment of pancreatitis by indirectly inhibiting activation of NF-κB.
