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

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.