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作 者:石欣[1] 裴斐[2] 高乃荣[1] Friess Helmut Kleeff Jorg Buchler Markus
机构地区:[1]东南大学附属中大医院普外科,南京210009 [2]湖北省黄石市中心医院普外科 [3]瑞士伯尔尼大学小岛医院内脏及移植外科
出 处:《中华实验外科杂志》2003年第2期166-167,共2页Chinese Journal of Experimental Surgery
基 金:国家人事部留学回国人员科研启动基金(7690004027)
摘 要:目的 了解P物质(SP)、神经激肽-1受体(NK-1R)及中性肽链内切酶(NEP)在胰腺癌细胞中表达。方法应用实时定量逆转录-聚合酶链反应(RQ-RT-PCR)技术,检测正常胰腺、胰腺癌组织和7株胰腺癌细胞中前速激肽原A(PPT-A)、NK-1R和NEP的mRNA表达,应用Westernblot检测NK-1R和NEP的蛋白水平。结果正常胰腺组织PPT-A的mRNA表达水平为0.430 0±0.464 7,胰腺癌组织中为1.790 0±1.833 1(P<0.05);正常胰腺NK-1R的mRNA表达水平为0.088 2±0.086 8,胰腺癌组织中为2.154 5±2.103 1(P<0.01);正常胰腺组织NEP的mRNA表达水平为3.234 7±6.301 0,胰腺癌为8.606 9±8.703 2(P>0.05)。Western Blot结果发现,胰腺癌组织中NK-1R蛋白也过度表达,而NEP的蛋白水平未相应上调。结论 胰腺癌组织中SP和NK-1R都明显上调,而SP的降解酶——NEP未相应上调,这表明胰腺癌组织中SP的产生与灭活的平衡被打破,产生过多的SP,发挥过度的生物学效应。Objective To investigate the expression of substance P (SP), neurokinin-1 receptor (NK-1R) and neutral endopeptidase (NEP) in human pancreatic cancer. Methods The expression of preprotachykinin A (PPT-A), NK-1R and NEP mRNA were investigated by real time quantitative reverse transcription polymerase chain reaction (RQ-RT-PCR) in normal pancreas, pancreatic cancer tissues and seven pancreatic cancer cell lines. The protein of NEP and NK-1R were analyzed using western blot analysis. Results The level of PPT-A mRNA in normal pancreas was 0.430 0 ± 0.464 7 and 2.154 5 ± 2.103 1 in pancreatic cancer tissues, thus pancreatic cancer tissues had a 4-fold increase in PPT-A mRNA levelsover normal pancreas ( P < 0. 05) ; NK-1R mRNA was 0. 0882 ± 0. 0868 in normal pancreas and 2.154 5 ± 2. 103 1 in pancreatic cancer tissues ( P < 0. 01); NEP mRNA in normal pancreas was 3.234 7 + 6. 301 0 and 8.606 9 ± 8. 703 2 in pancreatic cancer. Statistical analysis showed there was no significant difference between normal pancreas and pancreatic cancer tissues ( P > 0. 05 ). Western blot revealed NK-1R protein level was overexpressed in pancreatic cancer, while NEP were comparable between normal pancreas and pancreatic cancer tissue. Conclusion Together with our studies, enhanced expression of PPT-A and NK-1R, simultaneously with failure to upregulate NEP, disrupts the balance of neuropeptide loops and change pathoclinical aspect of pancreatic cancer.
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