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大鼠胰腺导管上皮细胞中白介素-1受体相关激酶-M的表达及意义
引用本文:陈珂玲,周翔宇,李园,周总光,周斌,姜晶晶,陈利辉. 大鼠胰腺导管上皮细胞中白介素-1受体相关激酶-M的表达及意义[J]. 中国微循环, 2009, 13(4): 272-276
作者姓名:陈珂玲  周翔宇  李园  周总光  周斌  姜晶晶  陈利辉
作者单位:1. 四川大学生物治疗国家重点实验室消化外科研究室,四川成都,610041
2. 四川大学华西医院普外科,四川成都,610041
基金项目:国家自然科学基金重点项目 
摘    要:目的探讨白介素-1受体相关激酶-M(IRAK-M)在胰腺导管上皮细胞(PDEC)中的表达状况及其在急性胰腺炎发病过程中的临床意义。方法脂多糖(LPS)刺激原代培养大鼠胰腺导管上皮细胞,实时荧光定量聚合酶链式反应(RT—PCR)技术,分别检测第2、6、12、24h刺激组和对照组IRAK—M,Toll样受体-4(TLR-4)及下游炎性细胞因子的mRNA表达量。结果IRAK-MmRNA在胰腺导管上皮细胞中呈阳性表达,与对照组相比,呈现出先降低后明显升高的趋势,于12h时达到峰值;与此相反,TLR4在刺激发生前期迅速上调,12—24h回落至基线水平。结论在LPS诱导的胰腺导管上皮细胞中,IRAK—M的表达具有一定的滞后性。IRAK—M可能通过调控TLR信号通路参与急性胰腺炎的发病过程。

关 键 词:IRAK-M  胰管上皮  先天免疫  急性胰腺炎

Expression and Significance of Interleukin-1 Receptor Associated Kinase-M on Rat Pancreatic Duct Epithelial Cells
CHEN Ke-ling,ZHOU Xiang-yu,LI Yuan,ZHOU Zong-guang,ZHOU Bin,JIANG Jing-jing,CHEN Li-hui. Expression and Significance of Interleukin-1 Receptor Associated Kinase-M on Rat Pancreatic Duct Epithelial Cells[J]. Journal of Chinese Microcirculation, 2009, 13(4): 272-276
Authors:CHEN Ke-ling  ZHOU Xiang-yu  LI Yuan  ZHOU Zong-guang  ZHOU Bin  JIANG Jing-jing  CHEN Li-hui
Affiliation:CHENKe-ling, ZHOU Xiang-yu, LI Yuan, ZHOU Zong-guang, ZHOU Bin, JIANG Jing-jing, CHEN Li-hui.( Digestive Surgery Research Section, Sichuan University, Chengdu 610041, China)
Abstract:Objective To study the expression of Interleukin-1 receptor associated kinase-M ( IRAK- M) on rat panceatic duct epithelial cells (PDEC) and its clinical significance involved in acute pancreatitis. Methods Primary cultured panceatic duct cells were divided into two groups, stimulated group and control group. The mRNA expression of IRAK-M, Toll like receptor-4 and downstream inflammation factors were detected by Real-Time Polymerase Chain Reaction ( RT-PCR). Both stimulated group and the control group were examined at the 2nd, 6th, 12th and 24th hour. Results The mRNA expression of IRAK-M was positive on pacreatic duct epithelial cells, which was significantly higher than control ceils at the 12th and 24th hour after being stimulated by lipopolysaceharide (LPS). IRAK-M mRNA expression decreased at the first 6 hours and then reached its peak at the 12th hour. TLR-4 mRNA primarily rose quickely, then decreased to baseline at the 12th hour. Conclusion The activation of IRAK-M was delayed in the pancreatic duct epithelial cells. IRAK-M may take part in the pathogenesis and development of acute pancreatitis through regulating TLR signaling way.
Keywords:IRAK-M
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