目的:探讨在急性胰腺炎中通过调控Gli1信号后观察炎性细胞因子IL-6的表达变化及意义.方法:本实验将C57小鼠随机分为3组:对照组、模型组、抑制组.雨蛙素腹腔注射诱导急性胰腺炎模型,HE染色、检测淀粉酶水平证明模型造模成功,用RT-qPCR、Western blot检测Gli1在胰腺、肝、小肠、肺、肾组织的表达.用ELISA方法检测炎性细胞因子IL-6.结果:雨蛙素腹腔注射诱导急性胰腺炎模型,HE染色、检测淀粉酶水平证明模型造模成功,用RT-qPCR、Western blot检测Gli1在胰腺、肝、小肠、肺、肾组织的表达.用ELISA方法检测炎性细胞因子IL-6.与对照组相比较,雨蛙素注射后的模型组各个组织(胰腺、肝、小肠、肺、肾组织)Gli1表达较对照组升高,再用Gant61(Gli特异性抑制剂)抑制Gli1后可见抑制组IL-6表达较模型组升高.结论:在急性胰腺炎症过程中,Gli1可能参与了AP过程中远隔组织损伤和修复过程,且gli1可能通过调控其下游的炎性细胞因子IL-6而发挥保护作用.%Objective:To investigate the expression and the significance of inflammatory cytokine IL-6 through regulating Gli1 in acute pancreatitis.Methods: In this study,C57 mice were randomly divided into three groups:control group,model group,inhibitor group.caerulein intraperitoneal injection induce acute pancreatitis model.Use HE staining and amylase to testify the model successfully.Use RT-qPCR,Western blot to detect the expression of Gli1 in the pancreas,liver,lung,kidney and intestine and ELISA method to detect inflammatory cytokines IL-6.Results: Compared with control group,the expression of Gli1 is higher in model group,then the expression of IL-6 increases in inhibitor group which uses Gant61 to suppress Gli1 compared with model group.Conclusion: Gli1 may involved in the process of the distant tissue injury and repair in acute pancreatitis and through regulate its downstream cytokines like IL-6 to play a protective role in acute pancreatitis.
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