Rosuvastatin inhibits TGF-beta1 expression and alleviates myocardial fibrosis in diabetic rats

Area of Science:

• Cardiology
• Pharmacology
• Diabetology

Background:

• Diabetic cardiomyopathy is a complex condition characterized by cardiac dysfunction in diabetic patients.
• Myocardial fibrosis and ventricular remodeling are key pathological features contributing to heart failure in diabetes.
• Transforming growth factor-beta1 (TGF-beta1) plays a crucial role in the development of cardiac fibrosis.

Purpose of the Study:

• To investigate the therapeutic effects of rosuvastatin on TGF-beta1 expression, cardiac fibrosis, ventricular remodeling, and cardiac function in a rat model of diabetic cardiomyopathy.
• To determine the dose-dependent effects of rosuvastatin on these pathological markers.

Main Methods:

• Twenty-seven diabetic rats, induced by streptozotocin, were divided into three groups: diabetic control, low-dose rosuvastatin (Ros-L), and high-dose rosuvastatin (Ros-H).
• Intervention groups received oral rosuvastatin at 2 mg/kg/d and 5 mg/kg/d for 10 weeks.
• Measurements included glycosylated hemoglobin (HbA1c), creatine phosphokinase isoenzyme (CK-MB), plasma brain natriuretic peptide (BNP), myocardial collagen volume fraction (CVF), left ventricular mass index (LVWI), and TGF-beta1 (mRNA and protein).

Main Results:

• Rosuvastatin treatment significantly reduced CK-MB levels compared to the diabetic group.
• The drug alleviated myocardial fibrosis and fibroplastic proliferation.
• Compared to the control group, the diabetic group exhibited higher LVWI, BNP, CVF, and TGF-beta1 levels, which were reduced by rosuvastatin treatment in a dose-dependent manner.

Conclusions:

• Rosuvastatin effectively reduces TGF-beta1 expression in a dose-dependent manner.
• Rosuvastatin inhibits the development of myocardial fibrosis and improves cardiac function in diabetic cardiomyopathy.
• These findings suggest rosuvastatin as a potential therapeutic agent for managing diabetic cardiomyopathy.