| Acute pancreatitis is a disease of variable severity in which some patients experience mild, self-limited attacks, whereas others manifest a severe, highly morbid, and frequently lethal attack. The events that regulate the severity of acute pancreatitis are, for most part, unknown. Most of scholars support the theory about activation of trysin. But, now it is generally believed that the earliest events in acute pancreatitis occur within acinar cells and result in acinar injury. Subsequently, the recruitment of inflammatory cells and generation of inflammatory mediaters are believed to result in acinar cells injury and systemic inflammatory response syndrome. A number of evidence have shown, in systemic inflammatory response syndrome of severe acute pancreatitis, leukocytes and leukocytes-derived products contribute to pancreatic and systemic injury. Many investigations have been tried to study those cytokines that regulate the activation of leukocytes, and block the occurrence of systemic inflammatory response syndrome. Recent studies have suggested that chemokines were probably important inflammatory cytokines in acute pancreatitis with local and systemic complications and may play an important pro-inflammatory role in regulating the severity of pancreatitis and associated lung injury. To clarity the role mat chemokine play in early acute pancreatitis, we examined the expression of CINC and MCP-l/JE in pancreas in severe and mild experimental models of rats with acute pancreatitis, and clarify the potential role of CINC and MCP-l/JE on the pathogenesis in early acute pancreatitis. In addition, the effect on anti-inflammatory, antiallergy and regulation of immune function of oxymatrine has been found in a lot of studies. The production of cytokines such as TNF and IL-6 can be inhibited by oxymatrine. The purpose of the study was to investigate the therapeutic effects of anti-inflammatory and regulation of immune function in experimental severe acute pancreatitis. So we can search for a drug of effective and safe.1. Induction of severe and mild experimental models of rats with acute pancreatitisObjective: To establish severe and mild experimental models of rats with acute pancreatitis(AP) by retrograde cholangiopancreatic duct infusion of different concentration of sodium taurocholate. Methods: Sixty-four rats were randomly devided into three groups: sham operation(SO)group> 0.5% sodium taurocholate(0.5%ST)group and 5% sodium taurocholate(5%ST)group. AP was induced by retrograde cholangiopancreatic duct infusion of 0.5% and 5% sodium taurocholate solution . Enzymatic method was applied for determination of the activity of serum amylase(Amy) blood glucose(GLU)and creatinine(Cr)level. Serum calcium(Ca2+)level was detected with chemistry chromatometry. Glutamic-pyruvic transaminase enzyme(GPT)level was tested with rate method. Death rate and histologic features of pancreas were evaluated. Results: Death rate were 0 and 35% in 0.5% ST and 5% ST group. Compared with the SO group, Amy was increased(p< 0.01)and pancreatic edema was found in 0.5% ST group. GLIK Cr and GPT were not markedly different from the SO group. The model was characteristic of mild acute pancreatitis(MAP). Amy GLLK GPT and Cr were significantly increased(p<0.05 p <0.01)and Ca2+ was decreased(p<0.05 p<0.01)in 5% ST group. The pathological changes of swelling and necrosis were found in pancreatic constitution. The model was characteristic of severe acute pancreatitis(SAP). Conclusion: MAP and SAP can be induced by retrograde cholangiopancreatic duct infusion of 0.5% and 5% sodium taurocholate.2. The role of CINC and MCP-l/JE in the pathogenesis of early acute pancreatitisObjective To explore the potential role of CINC and MCP-l/JE on the pathogenesis in early acute pancreatitis(AP). Methods Fifty-four rats were randomly devided into three groups: sham operation(SO) 3h, 6h, 12h group> Mild acute pancreatitis (MAP)3h, 6h, 12h group and severe acute pancreatitis(SAP) 3h, 6h 12h group. MAP and SAP were induced by retrograde infusion of 0.5 % or 5... |
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