摘要
目的建立糖尿病动物模型,研究CD59基因点突变与大鼠2型糖尿病的相关性。方法将Wistar大鼠随机分为正常组、双高饮食组和模型组。采用链尿佐菌素(STZ)制备糖尿病模型,设计MRCD59寡核苷酸探针(MRCD59X38 C39 W40 K41 H42 X43 X44 C45 X46),与大鼠肝、肾、胰组织进行原位杂交,以检测大鼠CD59基因点突变。同时采用免疫组化(SABC)法检测正常CD59在大鼠组织中表达情况。结果成功建立2型糖尿病大鼠模型。寡核苷酸探针及SABC证实双高饮食组及模型组大鼠组织正常CD59表达降低,而突变的RCD59增高,与正常组比较(P<0.01)有显著差异。结论RCD59基因突变与糖尿病密切相关。
Objective To construct rat model of type 2 diabetes and to explore the relationship between mutant CD59 gene and vascular proliferation of diabetes mellitus. Methods Rats were divided into three groups： control group, double highness （high sugar and high fat） group, and model group （constructed with SIZ）. In order to test rat mutant CD59 gene, mutant RCD59 oligonucleotides （MRCD59：X38 C39 W40 K41 H42 X43 X44 CA5 X46） were designed and in-situ hybridized with the rat tissue sections. Immunohistochemistry method （SABC） was used to test the expression status of normal CD59 protein in rat tissues. Results Rat model of type 2 diabetes had been successfully con- structed. Mutant CD59 showed positive expression by hybridization in-situ and SABC in double highness group and model group, which was significant difference as compared with that of control group （ P 〈 0.01）. Conclusion Mutant CD59 positive expression is related with type 2 diabetes mellitus.
出处
《免疫学杂志》
CAS
CSCD
北大核心
2007年第1期23-25,29,共4页
Immunological Journal
基金
国家自然科学基金资助项目(30170893)
关键词
CD39
基因突变
糖尿病
血管硬化
寡核苷酸探针
CD59
Site-directed mutagenesis
Diabetes
Vascular proliferation
Oligonucleotide
