Ellagic Acid Attenuates Oxidative Stress and Improves Cardiovascular Function Following Myocardial Infarction in Ovariectomized Rats.
LL, G., IV, A., EF, N., DSS, L., VS, L., AA, P., PW, E., SA, d.A., & GR, d.A. (2026). Ellagic Acid Attenuates Oxidative Stress and Improves Cardiovascular Function Following Myocardial Infarction in Ovariectomized Rats.. Journal of cellular and molecular medicine. https://doi.org/10.1111/jcmm.71262
LL G, IV A, EF N, DSS L, VS L, AA P, et al. Ellagic Acid Attenuates Oxidative Stress and Improves Cardiovascular Function Following Myocardial Infarction in Ovariectomized Rats.. Journal of cellular and molecular medicine. 2026; doi: 10.1111/jcmm.71262
LL G, IV A, EF N, et al. Ellagic Acid Attenuates Oxidative Stress and Improves Cardiovascular Function Following Myocardial Infarction in Ovariectomized Rats.[J]. Journal of cellular and molecular medicine. 2026. DOI: 10.1111/jcmm.71262.
@article{ll2026,
author = {Gonçalves LL and Alves IV and Nicoli EF and Lima DSS and Lemos VS and Peluso AA and Endlich PW and de Almeida SA and de Abreu GR},
title = {Ellagic Acid Attenuates Oxidative Stress and Improves Cardiovascular Function Following Myocardial Infarction in Ovariectomized Rats.},
journal = {Journal of cellular and molecular medicine},
year = {2026},
doi = {10.1111/jcmm.71262},
note = {PMID: 42363416},
}
TY - JOUR AU - Gonçalves LL AU - Alves IV AU - Nicoli EF AU - Lima DSS AU - Lemos VS AU - Peluso AA AU - Endlich PW AU - de Almeida SA AU - de Abreu GR TI - Ellagic Acid Attenuates Oxidative Stress and Improves Cardiovascular Function Following Myocardial Infarction in Ovariectomized Rats. T2 - Journal of cellular and molecular medicine PY - 2026 DO - 10.1111/jcmm.71262 AN - PMID:42363416 ER -
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.