I-Aβ1基因表达与小鼠膜性肾小球肾炎  

I-Aβ1 GENE EXPRESSION AND MOUSE MEMBRANOUS GLOMERULONEPHRITIS

作　　者：张旭[1] 高岑[1] 余绍兰[1] 马跃荣[1] 

机构地区：[1]泸州医学院病理教研室,四川泸州646000

出　　处：《泸州医学院学报》2009年第3期218-221,共4页Journal of Luzhou Medical College

摘　　要：目的:探讨I-Aβ1基因与实验性小鼠膜性肾小球肾炎发病之间的相关性。方法:复制并鉴定小鼠膜性肾小球肾炎动物模型,提取实验组和对照组总RNA,实时荧光定量PCR检测I-Aβ1基因mRNA表达量。结果:模型组I-Aβ1基因mR-NA表达量明显高于N-BSA组、NS组和空白对照组(P<0.01)差异有统计学意义;N-BSA组、NS组和空白对照组彼此之间的差异无统计学意义。结论:I-Aβ1基因过量表达参与了实验性小鼠膜性肾小球肾炎发病过程,可能是通过I-Aβ1基因转录、翻译活性上调使小鼠对外源性抗原反应性增强,促进了小鼠膜性肾小球肾炎发生。Objective：To study the relationship between I-Aβ1 gene and the pathogenesis of membranous glomerulonephritis in experimental mouse. Methods：The animal model of MGN was reproduced and identified in mouse, then the total RNA of experimental group and control group was extracted. After I-Aβ1 gene was extracted, spleen I-Aβ1 mRNA expression was detected by real time fluorescent quantitation PCR. Results： I-Aβ1 gene mRNA expression in model group was remarkably higher than that in group N-BSA, group NS and blank group （P〈0.01）, but there wasn＇t statistic significance among group N-BSA, group NS and blank group. Conclusion：I-Aβ1 gene overexpression may participate in the pathogenetic process of MGN in experimental mice; its potential nosogenesis is the up-regulation of I-Aβ1 genetic transcription and translation to promote antigen-reactive ability and morbility of MGN.

关 键 词：I—Aβ1 实时荧光定量PCR 膜性肾小球肾炎 

分 类 号：R363.21[医药卫生—病理学]