Studies Of Therapeutic Effects Of Tetramethylpyrazine On Experimental Acute Pancreatitis And Its Mechanism

Objective: To study the effects of TMP on experimental AP and to further explore its mechanism. Methods: By using improved Chetty methods, the rat model of severe acute pancreatitis(SAP) was prepared. After peritoneal injection administration of TMP, the changes of sera liver and kidney functions, amylzyne(AMY), C-reactive protein(CRP) and interleukines levels during the different period were observed, and the histological examinations were done at the same time. The rat model of acute edematous pancreatitis(AEP) was prepared by peritoneal injection of cerulein, and the treatment of AEP was done by the same injection of TMP. The apoptosis of pancreatic acinar cell was detected by triphosphate-biotin nick-end labeling(TUNEL). The expression of Bax gene was detected by immunohistochemistry method. And the same time, the changes of sera interleukines,CRP and amylzyme levels were observed. And the histological examination of pancreas, lung, liver, ren, heart and small intestine was done at the time. Resu Its: By the improved Chetty method, the rat model of SAP with multiplicate organ disfunction syndrome(MODS) complication was successful prepared. The interleukines and CRP levels were gradually increased along with the disease serverity. By peritoneal injection of cerulein for AEP, the significant cell apoptosis was observed in the pancreatic acinar cell with AEP. After treatment with TMP, the expression of IL-6, TNF- α , CRP and so on was inhibited by TMP, but the expression of IL-10 would not be promoted. TMP could upregulate the expression of pro-apoptosis Bax gene and promoted the apoptosis of the pancreatic acinar cell with AEP. TMP could relieve the change of pancreatic pathomorphism and the injery of multiplicate organ. The injury of pancreatic sub-cell structure could be seldom seen. TMP has protective effect on pancreatic cell in experimental AP and sub-cell structure. Conclusion: The mechanism of TMP on AP is to restrain the expression of IL-6, TNF- α , CRP and upregulate the expression of pro-apoptosis Bax gene and promote the apoptosis of the pancreatic acinar cell with AEP.