Aim: To investigate the pathogenesis of diabetic cardiomyopathy. The differences of myocardial tissue gene expressions among diabetic group, control group, and high dose melatonin group were compared by using rat genomewide spectrum illumina beads chip. Methods: Divide 12 SD rats into 3 groups, control group, streptozotocin (STZ) induced diabetic group, and diabetic and melatonin group. Extract mRNA from the myocardial tissue, transcript it into cDNA, hybridize the cDNA with gene chips, and then statistically analyze the results of gene chip scanning. Results: Compared with the control group, the protein metabolism related gene expression significantly downregulated while apoptosis relevant gene expression upregulated in diabetic rats. Compared with the diabetic group, glucose and protein metabolism related genes expression in high dose melatonin group significantly increased while apoptosis and oxidative stress genes decreased in melatonin group. Conclusion: The results of gene chip analysis showed that glucose and protein metabolism, oxidative stress and apoptosis played important roles in the pathogenesis of diabetic cardiomyopathy.
References
[1]
M. Hamblin, D. B. Friedman, S. Hills, et al. Alteration in the diabetic myocardial proteome coupled with increased myocar- dial oxidative stress underlies diabetic cardiomyopathy. Journal of Molecular and Cellular Cardiology, 2007, 42(4): 884-895.
[2]
Y. Weng, F. Shen, J. Li, et al., Expression changes of mitogen- activated protein kinase phosphatase-1 (MKP-1) in myocardium of streptozotocin-induced diabetic rats. Experimental and Clini- cal Endocrinology & Diabetes, 2007, 115(7): 455-460.
[3]
H. Nie, J. L. Wu, M. Zhang, et al., En-dothelial nitric oxide syn- thase-dependent tyrosine nitration of prostacyclin synthase in diabetes in vivo. Diabetes, 2006, 55(11): 3133-3141.
[4]
J. W. Hartog, A. A. Voors, S. J. Bakker, et al., Ad-vanced glyca- tion end-products (AGEs) and heart failure: Pathophysi-ology and clinical implications. European Journal of Heart Failure, 2007, 9(12): 1146-1155.
[5]
R. Marfella, C. Di Filippo, M. Por-toghese, et al., The ubiquitin- proteasome system contributes to the inflammatory injury in is- chemic diabetic myocardium: The role of glycemic control. Car- diovascular Pathology, 2009, 18(6): 332-345.
[6]
H. Miyazaki, N. Oka, A. Koga, et al., Comparison of gene ex- pression profiling in pressure and volume overload-induced myocardial hypertrophies in rats. Hypertension Research, 2006, 29(12): 1029-1045.