Targeting Apoptosis in the Heart of Streptozotocin-Induced Diabetic Rats

Abstract

Objectives: The aim of the current study was to address the issue of cardiomyocyte apoptosis as a possible contributor in the development of diabetic cardiomyopathy and whether it would be possible to suppress this apoptosis by the use of a peroxisome proliferator-activated receptor (PPAR)-α agonist (fenofibrate) or a PPAR-γ agonist (rosiglitazone). Methods: Ten normal male albino rats (group I) were injected intraperitoneally (IP) by a single dose of saline and served as a control for group II. Thirty male albino rats were made diabetic by IP streptozotocin (STZ) injection and were divided into 3 groups: group II (nontreated diabetic rats), groups III and IV (diabetic rats treated with PPAR-γ agonist (rosiglitazone), and PPAR-α agonist (fenofibrate) respectively, for 12 weeks starting 1 week following STZ injection. Results: The studied drugs decreased left ventricular to body weight ratio and cardiac: caspase-3, tumor necrosis factor-α, hydroxyproline, free fatty acids (FFAs) as well as triglycerides (TGs) and improved oxidative stress parameters as well as left ventricular papillary muscle developed tension (DT). Conclusions: The results of the current study support the hypothesis that apoptosis plays a key role in the pathophysiology of diabetic cardiomyopathy and demonstrate that the use of PPAR-α and -γ agonists might have a protective role against diabetic cardiomyopathy.