Ellagic acid (30 mg/kg) improved hemodynamic function, reduced collagen deposition, decreased MMP-8 and IL-6, and enhanced NO bioavailability in ovariectomized rats following myocardial infarction.
Does ellagic acid improve cardiovascular function and attenuate cardiac fibrosis in ovariectomized rats following myocardial infarction?
In a rat model of estrogen deficiency, ellagic acid mitigated post-myocardial infarction cardiac fibrosis and ventricular dysfunction via antioxidant and anti-inflammatory effects.
ABSTRACT 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.
Gonçalves et al. (Mon,) conducted a other in Myocardial infarction with oestrogen deficiency. Ellagic acid was evaluated on Hemodynamic parameters, collagen deposition, infarct size, MMP-8, NO, superoxide anion and inflammatory cytokines. Ellagic acid (30 mg/kg) improved hemodynamic function, reduced collagen deposition, decreased MMP-8 and IL-6, and enhanced NO bioavailability in ovariectomized rats following myocardial infarction.
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