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