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作 者:徐颖婕[1] 李冰[1] 王培林[1] 褚现明[2] 杨帆[1] 吕丛仪[1]
机构地区:[1]青岛大学医学院生物学教研室,青岛266021 [2]青岛大学医学院附属医院心内科,青岛266000
出 处:《现代免疫学》2013年第4期279-284,共6页Current Immunology
基 金:国家自然科学基金(81001346);山东省医药卫生科技发展计划项目(2011HZ023);青岛市公共领域科技支撑计划项目(2012-1-3-5-(4)-nsh);山东省科学技术发展计划项目(2012YD18035)
摘 要:本文主要探讨了CD59基因转染对小鼠动脉粥样硬化的作用。将30只ApoE基因缺失(ApoE-/-)小鼠随机分为3组:对照组、0.5ml CD59处理组、1.0ml CD59处理组。在高脂饮食的同时进行药物干预。12周后,RT-PCR检测全血中CD59mRNA水平,western blot检测组织中CD59蛋白表达量。检测血清生化指标,并取主动脉根部制作石蜡切片,HE染色观察动脉粥样硬化斑块形成情况。动脉粥样硬化小鼠模型构建成功。CD59具有一定的降低血脂水平和抑制动脉粥样硬化斑块形成的作用,且CD59表达量与动脉粥样硬化发展程度成负相关。证明CD59基因能够在一定程度上减缓甚至抑制动脉粥样硬化的发生发展,可作为动脉粥样硬化靶向治疗的一个有效靶点。To study the effects of CD59 gene on occurrence and development of atherosclerosis , 30 ApoE gene deletion (ApoE (-/-))mice were randomly divided into three groups: control group, 0. 5ml CD59 treated group, and 1. 0ml CD59 treated group. During the entire experiment course, all the mice were received high-fat diet. At the end of the 12'h week, CD59 mRNA level was detected by RT-PCR and CD59 protein expression index was determined by Western blot, and blood fat levels were examined. Atherosclerotic plaques in the aortic root were examined by routine histology of HE staining. The results showed that mouse atheroselerosis model was successfully established. CD59 gene could lower blood fat level and inhibit atherosclerotic plaques formation, and these effects were negatively correlated with expression level of CD59 gene. Taken together, these results suggest that C59 gene therapy may delay, or even inhibit the development of atherosclerosis.
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