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

Di Yi Jun Yi Da Xue Xue Bao. 2004 Jul;24(7):827-8, 831.
[Article in Chinese]

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.

Publication types

  • English Abstract

MeSH terms

  • Animals
  • Captopril / pharmacology*
  • Captopril / therapeutic use
  • Cardiomyopathies / drug therapy
  • Cardiomyopathies / metabolism*
  • Diabetes Mellitus, Experimental / complications*
  • Diabetes Mellitus, Experimental / metabolism
  • Energy Metabolism / drug effects*
  • Male
  • Myocardium / metabolism*
  • Oligonucleotide Array Sequence Analysis
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Captopril