中文摘要：

目的探讨重症急性胰腺炎（ SAP）早期炎症因子的分泌与JAK2/STAT3信号通路之间的关系。方法以4%牛磺胆酸钠胰胆管逆行注射诱导大鼠 SAP模型。32只雄性SD大鼠随机分为4组：对照组和SAP造模组（6、12、18 h），每组8只。动态测定各组血清淀粉酶（ AMY ）和胰脂肪酶（ LPS）、血钙（ Ca2＋）水平；光镜下观察胰腺病理变化；ELISA法检测血清肿瘤坏死因子-α（ TNF-α）、白介素-1β（ IL-1β）及白介素-18（IL-18）表达情况；RT-PCR和Western blot法分别检测胰腺组织中JAK2和STAT3在胰腺中的表达水平变化。结果各SAP造模组血清学指标水平、TNF-α、IL-1β及IL-18均明显高于对照组；病理学显示胰腺组织随病情进展逐步加重；SAP造模组胰腺JAK2和STAT3基因和蛋白的表达均明显增高，且JAK2和STAT3表达变化与胰腺组织的严重程度相一致。结论 SAP早期促炎因子过度表达是病情进展的损伤因子，可能通过诱导 JAK2/STAT3信号通路的活化，加重SAP早期器官损伤程度。

英文摘要：

Objective To investigate the relationship between proinflammatory cytokines and JAK2/STAT3 signal pathway in early severe acute pancreatitis. Methods The rat model of SAP was reproduced by retrograde infusion of 4% sodium taurocholate into the biliopancreatic duct. Thirty-two male SD rats were randomly assigned into 4 groups （8 each）：normal control group, SAP 6 h, 12 h and 18 h groups. The levels of serum amylase, lipase and calcium level were measured dynamically, pathological changes in pancreas was evaluated. The concentrations of TNF-α, IL-1β and IL-18 were determined by ELISA, and the expressions of JAK2 and STAT3 protein and mRNA in pancrease was also determined by Western blot and RT-PCR. Results The SAP module groups serology level, TNF-α, IL-1βand IL-18 were significantly higher than those in NC group. The microscopic pancreas injuries were gradually aggravated with disease progression. The expression of JAK2 and STAT3 gene and protein in experimental groups were significantly increased compared with NC group, and reached the peak in 18h group. Conclusion Se-vere acute pancreatitis proinflammatory cytokines overexpression is damage factor progression of disease, which may activate the JAK2/STAT3 signaling pathway, aggravating the organ injury in early stage of severe acute pancreati-tis.