ArticleJournal of cellular and molecular medicine2026
Ellagic Acid Attenuates Oxidative Stress and Improves Cardiovascular Function Following Myocardial Infarction in Ovariectomized Rats.
Article in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.