及时恢复胃肠动力，减少炎症反应有助于缓解重症急性胰腺炎向多器官功能衰竭发展，且有利于防止后期胰腺或胰周感染。钙依赖途径是启动胃肠运动的重要环节，钙敏感性途径即MLCP信号通路是引起平滑肌钙敏感性改变和其收缩的关键，而炎症介质是加重胃肠动力障碍的重要因素。蛋白激酶C加强的磷酸酶抑制剂17（CPI-17）是MLCP信号通路的枢纽，同时受到炎症介质的调节。我们前期研究证实中药验方柴芩承气汤可减少急性胰腺炎炎症介质释放，上调大鼠肠道平滑肌细胞钙依赖途径磷脂酶C-β1、蛋白激酶C-α表达，促进钙库释放钙，启动胃肠运动。我们推断柴芩承气汤降低该病炎症介质释放，恢复胃肠动力，还与肠道平滑肌细胞MLCP信号通路有关。本项目检测急性坏死性胰腺炎大鼠肠道平滑肌细胞MLCP信号通路相关蛋白及炎症介质表达的变化，研究其对该病肠道平滑肌细胞MLCP信号通路的影响。为深入阐明中药防治急性胰腺炎的作用机制获得新发现。

Prevention and improvement of gastrointestinal dismotility timely and reduction of inflammation were contributed to the prognosis of severe acute pancreatitis（SAP）,including alleviation of SAP developed into multiple organ failure and prevention of the development of pancreatic or peripancreatic infection in the late stage of SAP. Calcium-dependent pathway is a key link to start gastrointestinal motility, and calcium sensitivity pathway（MLCP signaling pathway） is an important way that causes the changes of calcium sensitivity and the contraction of intestinal smooth muscle. Inflammatory cytokines is an important part of exacerbation gastrointestinal dysmotility. Proteinkinase C-potentiated phosphatase inhibitor of l7 ku(CPI-17) is not the hub of the MLCP pathway, but also regulated by inflammatory cytokines. Our previous studies have confirmed prescription medicine Chaiqingchengqi decoction（CQCQD）can reduce the levels of inflammatory mediators, and can promote calcium store release of calcium and promote colonic smooth muscle contraction by increasing the expression of PhospholipaseC -β1 and protein kinase C –α of the alcium-dependent pathway in rats of severe acute pancreatitis. In the present study, we intend to investigate the effects of the CQCQD on the MLCP signaling pathway of intestinal smooth muscle cells through detection the changes of the expression of mRNA and related proteins, inflammatory cytokines in acute necrotizing pancreatitis rats intragastrically administered. This study is expected to further elucidate the role of Chinese medicine to prevent acute pancreatitis innovative mechanism has been found.