Investigation of the effect of quercetin on experimental traumatic cardiac injury in rats

TL;DR

This study finds that quercetin, especially at high doses, may protect rat hearts from trauma-induced injury by reducing oxidative stress and tissue damage.

Contribution

The novel finding is that quercetin at 40 mg/kg significantly reduces oxidative stress markers and histopathological damage in traumatic cardiac injury in rats.

Findings

Quercetin at 40 mg/kg significantly reduced malondialdehyde levels, indicating reduced oxidative stress.

Histopathological damage was mitigated in a dose-dependent manner, with the highest dose showing the most protection.

Quercetin's protective effects were not consistently observed in all biochemical markers like IL-1 and SOD.

Abstract

Cardioprotection is an important aspect of preventive medicine. Quercetin, a plant-derived flavonoid with antioxidant and anti-inflammatory properties, has been linked to reduced cardiovascular risk.

To investigate the cardioprotective effects of quercetin in rats with traumatic cardiac injury (TCI).

Fifty-two Wistar Albino rats were randomly divided into six groups: control (n = 7); TCI only (n = 9); TCI + DMSO (n = 6); and TCI + quercetin at 10, 20, or 40 mg/kg (n = 9 each). Quercetin or DMSO was given intraperitoneally at 0.5, 12, and 24 h after trauma. Cardiac trauma was induced by dropping a standardized weight on the chest. Serum biochemical parameters (GPx, SOD, IL-1, IL-33, sST2, MDA) were measured by ELISA, and histopathological damage was scored semiquantitatively. Data were analyzed using ANOVA or Kruskal–Wallis tests with p < 0.05 as significant.

GPx elevation was detected only at 10 and 20 mg/kg (vs. TCI; p < 0.05); 40 mg/kg was non-significant (p > 0.05). Overall, IL-1 differed among groups (p = 0.008), with no pairwise comparisons significant after correction (all p > 0.05). For IL-33, an overall group effect was observed (p = 0.025), while adjusted pairwise tests did not show a consistent between-group pattern (p > 0.05). In contrast, malondialdehyde (MDA) levels were significantly reduced, particularly at the highest dose of 40 mg/kg (p < 0.05). Superoxide dismutase (SOD) and soluble suppression of tumorigenicity-2 (sST2) levels showed no significant differences among groups (p > 0.05). Histopathological evaluation demonstrated that quercetin mitigated myocardial degeneration, inflammatory infiltration, edema, vascular congestion, hemorrhage, and necrosis in a dose-dependent manner, with the most pronounced protective effects observed at 40 mg/kg (p < 0.05).

Quercetin, especially at 40 mg/kg, may help prevent secondary cardiac injury after trauma by reducing oxidative stress and limiting histopathological damage. These results support quercetin's cardioprotective potential and warrant confirmation in larger preclinical models with broader designs.

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