急性胰腺炎是全世界最常见的急腹症之一，极易继发局部感染和脓毒血症，目前公认肠粘膜屏障破坏引起的细菌和内毒素移位是感染的主要原因。本课题组使用院内方剂抑胰合剂，经临床证明，可有效改善肠粘膜屏障，促进肠内营养48h早期实施。在随后的动物预实验中我们发现，JNK/c-Jun和Pi3k/Akt两条通路极有可能参与其中。因此我们提出抑胰合剂的调控作用与JNK/c-Jun和Pi3k/Akt双通路相关的科学假说。这两条通路对肠粘膜屏障的影响可能处于一种微妙的平衡状态，在急性胰腺炎时则此消彼长，引起肠粘膜屏障损伤，而抑胰合剂正是通过双向调节这两条通路，打断炎症因子和细菌、内毒素相互激活的恶性循环而起到治疗作用。本课题组拟通过JNK/c-Jun通路抑制剂（SP600125）和Pi3k/Akt抑制剂（Wortmannin）的干预来验证我们的假说，并尝试寻找抑胰合剂的作用靶点及分子机制，拓展中医药研究思路。

Acute pancreatitis is one of the most common acute abdominal diseases in the world, and can lead to local infection and sepsis easily. It's accepted widely that damage of intestinal mucosal barrier is the main cause of bacteria and endotoxin translocation. It has been proved by clinic that Yiyi mixture can improve the intestinal mucosal barrier and promote early enteral nutrition within 48h. And we found that JNK/c-Jun and Pi3k/Akt pathway is probably involved in the course in later animal experiments. Thus, we put forward the hypothesis that therapeutic effect of Yiyi mixture is associated with JNK/c-Jun and Pi3k/Akt signal pathway. The two pathways may be in a delicate balance in intestinal mucosal barrier，and be in disorder in acute pancreatitis, which further lead to intestinal mucosal injury. Yiyi mixture could inhibit the vicious circle of inflammatory cytokines, bacteria and endotoxin through adjustment of the two pathways. This research intends to verify our hypothesis through the intervention of the inhibitors of the two pathways-SP600125 and Wortmannin. We try to find the targets and molecular mechanism of Yiyi mixture, and expand the research of traditional Chinese medicine.