南方医科大学学报 ›› 2004, Vol. 24 ›› Issue (07): 827-828,831.

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卡托普利对糖尿病性心肌病大鼠心肌组织能量代谢和炎症反应的影响

陈刚, 林丽香, 庄维特, 姚瑾, 黄惠彬, 梁继兴, 张芳林, 温俊平, 李连涛, 林苗, 林庆明   

  1. 福建省立医院内分泌科, 福建, 福州, 350001
  • 出版日期:2004-07-20 发布日期:2004-07-20
  • 基金资助:
    收稿日期:2003-12-23。
    作者简介:陈刚(1971- ),男,2000年毕业于上海第二医科大学,博士,副主任医师,电话:0591-7557768-3015

Effects of captopril on myocardial tissue energy metabolism and inflammation in rats with diabetic cardiomyopathy

CHEN Gang, LIN Li-xiang, ZHUANG Wei-te, YAO Jin, HUANG Hui-bin, LIANG Ji-xing, ZHANG Fan-lin, WEN Jun-ping, LI Lian-tao, LIN Miao, LIN Qing-min   

  1. 福建省立医院内分泌科, 福建, 福州, 350001
  • Online:2004-07-20 Published:2004-07-20

摘要: 目的 探讨卡托普利保护心肌组织的作用机制。方法 (1)将糖尿病性心肌病大鼠分为对照组和治疗组,治疗组每天给予卡托普利1.5 mg/kg·b.w.,口服15 w;(2)从动物心肌组织中抽提mRNA,经逆转录分别用Cy3、Cy5荧光标记,获得两组动物来源的cDNA探针;(3)cDNA探针与基因表达谱芯片杂交,结果由扫描仪扫描并用软件进行分析统计。结果 (1)脂肪酸b氧化相关基因、线粒体电子质子偶联和氧化磷酸化相关基因、烟酰胺腺嘌呤二核苷酸磷酸(NADP)依赖的白三烯B4羟基脱氢酶基因在治疗组中表达明显上调。(2)二甲基精氨酸水解酶基因在干预治疗组中表达明显下调。结论 卡托普利可能通过改善病变心肌的能量供应、抑制炎症反应对糖尿病性心肌病心肌组织起保护作用。

Abstract: Objective To study the protective mechanism of captopril in diabetic cardiomyopathy by means of DNA microarray. Methods Rat models of diabetic cardiomyopathy were divided into test and control groups (n=5), and the rats in the test group were given oral captopril (1.5 mg/kg·b.w.) for 15 weeks. DNA microarray was prepared by blotting the PCR products of 4 000 rat cDNAs onto a specially treated glass slides. The probes were prepared by labeling the mRNA from the myocardial tissue of both control and test groups with Cy3-d UTP and Cy5-d UTP separately through reverse transcription. The arrays were then hybridized against the cDNA probes and the fluorescent signals scanned. Results The expression of genes in relation to fatty acid b oxidation, mitochondrial proton-electron coupling and oxidative phosphorylation, and that of dithiolethione-inducible gene-1 were up-regulated, while the dimethylarginine dimethylaminohydrolase gene expression was obviously lowered in the test group in comparison with those of the control group. Conclusion Captopril may protect the myocardial tissue through improving myocardial energy supply and depressing inflammatory reaction.

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