Effects of polydatin on attenuating ventricular remodeling in isoproterenol-induced mouse and pressure-overload rat...

Area of Science:

• Cardiovascular Research
• Pharmacology
• Biochemistry

Background:

• Ventricular remodeling is a pathological process contributing to heart failure.
• Isoproterenol and abdominal aortic banding are established models for inducing cardiac stress and remodeling.
• Neurohormonal activation, especially the rennin-angiotensin-aldosterone system (RAAS), plays a critical role in cardiac remodeling.

Purpose of the Study:

• To investigate the protective effects of polydatin against ventricular remodeling.
• To elucidate the mechanisms underlying polydatin's actions, focusing on neurohormonal pathways.

Main Methods:

• Animal models of cardiac remodeling were utilized: isoproterenol-induced in mice and abdominal aortic banding in rats.
• Cardiac weight index, cardiomyocyte size, and ventricular collagen volume were assessed.
• Levels of cyclic AMP, angiotensin II, aldosterone, tumor necrosis factor-α, and endothelin-1 were measured.
• Blood pressure was monitored in rats.

Main Results:

• Polydatin administration significantly reduced cardiac weight indexes in both mice and rats.
• In mice, polydatin lowered levels of cyclic AMP and angiotensin II.
• In rats, polydatin decreased cardiomyocyte size, aldosterone, tumor necrosis factor-α, angiotensin II, and endothelin-1 levels.
• Polydatin also reduced ventricular collagen volume and lowered blood pressure in rats.

Conclusions:

• Polydatin exhibits significant cardioprotective effects by attenuating ventricular remodeling.
• The beneficial actions of polydatin are linked to the inhibition of neurohormonal activation, particularly the rennin-angiotensin-aldosterone system.
• Polydatin demonstrates potential as a therapeutic agent for conditions involving cardiac remodeling.