AR42J细胞自分泌Shh信号参与雨蛙素诱导的急性胰腺炎  

Potential roles of autocrine Shh signal in caerulein-induced acute pancreatitis

作　　者：周翔宇 陈霞 黄娟 曾凡才[4] 

机构地区：[1]四川医科大学附属第一医院血管甲状腺外科 [2]四川医科大学附属第一医院消化内科 [3]四川医科大学附属第一医院病理科 [4]四川医科大学生物化学教研室,四川泸州646000

出　　处：《泸州医学院学报》2015年第6期533-536,共4页Journal of Luzhou Medical College

基　　金：国家自然科学基金资助项目(No:81100272);四川省科技厅基金资助项目(No:2014JY0004)

摘　　要：目的:观察Hedgehog信号在急性胰腺炎(AP)体外模型中的表达变化。方法:不同浓度的雨蛙素诱导大鼠胰腺腺泡细胞株AR42J,构建AP体外细胞模型,重组Shh作用于AR42J细胞。采用RT-PCR、Western-blot分别检测细胞Shh信号分子表达;ELISA检测上清Shh水平。结果:与对照组相比,雨蛙素诱导组Shh的m RNA和蛋白水平表达明显升高,细胞自分泌Shh水平也明显升高,呈雨蛙素浓度依赖性。重组Shh刺激后,Shh相关信号Shh、Gli1和Ptch1表达呈浓度依赖性地升高。结论:在雨蛙素诱导的AR42J细胞,自分泌的Shh信号参与急性胰腺炎的发病机制。Objective： To investigate the potential roles of Hedgehog signal in caerulein-induced acute pancreatitis. Methods： Different doses of caerulein were used to induce acute pancreatitis in pancreatic acinar cell lines, AR42 J. Cells and conditioned medium were collected after 24 hours. The expression of Shh was detected by RT-PCR and Western-blot respectively, and levels of Shh in conditioned medium were measured by ELISA. After treatment of AR42 J cells with recombinant Shh N-terminal peptide, the expression of the hedgehog signaling components, Shh, Gli1, and Ptch1 were evaluated by RT-PCR. Results： Caerulein induced expression of Shh at both m RNA and protein levels in pancreatic AR42 J cell lines in a dose dependent manner, so did the soluble Shh in the conditioned medium. Recombinant Shh stimulated the expression of the hedgehog signaling components, Shh, Gli1, and Ptch1. Conclusion： Caerulein up-regulated the expression of Shh in AR42 J cells,and recombinant Shh stimulated the expression of hedgehog signaling components, Shh, Gli1, and Ptch1,suggesting autocrine Shh signal may contribute to the pathogenesis of acute pancreatitis.

关 键 词：雨蛙素 AR42J 急性胰腺炎 Sonic Hedgehog信号 

分 类 号：Q576[生物学—生物化学]