Changes in expression of adrenomedullin in the myocardium of streptozotocin-induced diabetic rats.
- Author:
Rong-xin HE
1
;
Chuan-long GU
;
Fang SHEN
;
Xiao-ming ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Adrenomedullin; analysis; Animals; Blood Glucose; analysis; Cardiomyopathies; etiology; Diabetes Mellitus, Experimental; complications; metabolism; Female; Immunohistochemistry; Myocardium; chemistry; ultrastructure; Rats; Rats, Sprague-Dawley; Streptozocin
- From: Chinese Medical Journal 2007;120(3):187-191
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDAdrenomedullin is a potent vasodilating peptide and involved in many cardiovascular diseases. However, whether adrenomedullin is involved in the pathogenesis of diabetic cardiomyopathy is still unknown. Our aim was to characterize the expression pattern of adrenomedullin in the myocardium of streptozotocin-induced diabetic rats.
METHODSThe weight, blood glucose, and urine glucose of 20 streptozotocin-induced diabetic rats were measured before and after model induction in the diabetic and control groups. The alteration of the adrenomedullin expression was explored in the left ventricular myocardium in both groups by immunohistochemistry. Changes in heart ultrastructure were also analyzed by using hemotoxylin and eosin staining and transmission electron microscopy. All data were analyzed by the independent samples t test.
RESULTSThe data of weight, blood glucose, and urine glucose had no significant difference between the control and the diabetic groups before animal model induction. Four weeks after the induction of diabetes, the differences between the two groups in weight, blood glucose, and urine glucose were distinct. When compared with the control group, the diabetic group showed ultrastructural changes including hypertrophy, fibrosis, myofibrillar disarrangements, mitochondrial disruption, and increase in nuclear membrane invaginations. A significant decrease of adrenomedullin expression was also observed in cardiac myocytes of the diabetic rats (P < 0.01).
CONCLUSIONSOur study provides experimental evidence that hyperglycemia could damage cardiac myocytes. Down-regulation of cardioprotective peptide adrenomedullin in the myocardium of streptozotocin-induced diabetic rats may contribute to the diabetic cardiomyopathy and left ventricular dysfunction.