Assessment of cardiac inflammation and remodeling during the development of streptozotocin-induced diabetic cardiomyopathy in vivo: A time course analysis

In this study, we examined cardiac inflammation, fibrosis and left ventricular (LV) function during the development of streptozotocin (STZ)-induced diabetic cardiomyopathy using an animal model of diabetes mellitus (DM). Diabetes was induced in 22 Sprague-Dawley rats by an intraperitoneal single inj...

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Bibliographic Details
Published in:International journal of molecular medicine 2013-07, Vol.32 (1), p.158-164
Main Authors: BECHER, P.M, LINDNER, D, FRÖHLICH, M, SAVVATIS, K, WESTERMANN, D, TSCHÖPE, C
Format: Article
Language:English
Subjects:
cardiac function
Cardiomyopathy
Cardiovascular disease
Catheters
Diabetes
diabetic cardiomyopathy
Genotype & phenotype
Heart failure
Heart rate
Hyperglycemia
Inflammation
Insulin
Laboratory animals
Oxidative stress
Pathogenesis
Protein expression
Proteins
remodeling
Rodents
Statistical analysis
Studies
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Summary:In this study, we examined cardiac inflammation, fibrosis and left ventricular (LV) function during the development of streptozotocin (STZ)-induced diabetic cardiomyopathy using an animal model of diabetes mellitus (DM). Diabetes was induced in 22 Sprague-Dawley rats by an intraperitoneal single injection of STZ (70 mg/kg). Non-diabetic animals served as the controls (n=6). LV function was documented using the conductance catheter technique 2 and 6 weeks after the induction of diabetes. Cardiac tissue was analyzed for cardiac immune cell infiltration, oxidative stress and remodeling in rats with STZ-induced diabetes at 2 different time points by immunohistochemistry. Cardiac function was significantly impaired in the diabetic animals. After 2 weeks, the induction of diabetes resulted in impaired cardiac function indexed by a decrease in systolic and diastolic LV function. This impairment of LV performance continued for up to 6 weeks after the STZ injection. This was associated with an increase in cardiac CD3+ and CD8a+ immune cell invasion and fibrosis, indexed by an increase in collagen content (p
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2013.1368