Ellagic Acid Attenuates Oxidative Stress and Improves Cardiovascular Function Following Myocardial Infarction in Ovariectomized Rats.

Oestrogen deficiency increases oxidative stress and reduces nitric oxide (NO) bioavailability, contributing to cardiac fibrosis following myocardial infarction (MI). This study investigated whether ellagic acid (EA), a natural antioxidant, attenuates post-MI cardiac fibrosis in ovariectomized rats by reducing oxidative stress and pro-inflammatory mediators. MI was induced by coronary artery ligation, and EA (30 mg/kg) was administered orally for 4 weeks. Hemodynamic parameters, collagen deposition, infarct size, matrix metalloproteinase-8 (MMP-8), NO, superoxide anion and inflammatory cytokines were assessed. MI resulted in ventricular dysfunction, increased collagen deposition and elevated levels of MMP-8, interleukin-6 (IL-6) and superoxide anion. EA treatment improved hemodynamic function, reduced collagen deposition, decreased MMP-8, IL-6 and superoxide anion, and enhanced NO bioavailability. These findings demonstrate that EA mitigates cardiac fibrosis and ventricular dysfunction through antioxidant and anti-inflammatory mechanisms, highlighting its potential as a cardioprotective compound in post-MI conditions under oestrogen deficiency.