期刊论文

中文

山东医药

1002-266X

2012

52

23

5-7

10.3969/j.issn.1002-266X.2012.23.002

81100212/H0215:国家自然科学基金 20114324120004:高等学校博士学科点专项科研基金 2012M511383:中国博士后科学基金 11C1094,08C743:湖南省教育厅科学研究项目 2011XQD24:南华大学***人才科研启动资助项目

本校为第一机构

目的 探讨心肌细胞缺氧复氧损伤时心肌缺血预适应表达上调蛋白1( Mipu1)启动子活性的变化及其作用.方法 按本课题组的常规方法复制心肌细胞缺氧复氧模型,先予缺氧(95％N2-5％CO2,无血清低糖DMEM)处理6h,再分别复氧(95％空气-5％ CO2,10％FBS-高糖DMEM)6、12、24h.采用MTT法检测心肌细胞活性,比色法测定心肌细胞LDH活性,双荧光素酶报告基因技术检测启动子PGL3-Mipu1活性,实时定量PCR法检测Mipu1 mRNA表达.结果 缺氧6h复氧(6、12、24 h)后心肌细胞活性减低,LDH释放增加,启动子PGL3-Mipu1活性增加,Mipu1 mRNA表达上调,且在缺氧6h复氧12 h时变化最明显.结论 Mipu1可能参与了心肌细胞的缺氧复氧损伤,...

Objective To investigate the changes and roles of Mipul promoter activity during cardiomyocytes hypoxia/ reoxygenation injury. Methods The cardiomyocytes H9c2 injury model was induced by hypoxia/reoxygenation, H9c2 cells were transferred to a hypoxic incubator that contained 95% N2-5% CO2 for 6 hs of hypoxia, and then were transferred to a normoxic incubator （95% air-5% CO2 ） for 6, 12 and 24 hs. The activity of H9c2 cells was detected by MTF method. Serum LDH activity was measured by chromatometry. PGL3-Mipul promoter activity was dectected ...