What question did this study set out to answer?

This study aims to evaluate the cardioprotective effects of hesperidin against deltamethrin-induced damage in rats.

April 7, 2026Journal of Cardiovascular Development and Disease0 citationsOpen Access

Protective Role of Hesperidin Against Deltamethrin-Induced Cardiovascular Structural Damage: Involvement of Caspase-3-Driven Apoptosis and Fibrosis Suppression in Rats

BGBurcu Gültekin HCHalime Tuba Canbaz HSHasan Basri Savaş

Key Points

This study aims to evaluate the cardioprotective effects of hesperidin against deltamethrin-induced damage in rats.
Thirty-two male Wistar Albino rats were divided into four groups: Control, DLM, DLM + HSP 100, and DLM + HSP 300.
Serum levels of ischemia-modified albumin, glucose, cholesterol, triglycerides, and HDL were analyzed at the end of the experiment.
Histopathological assessments were conducted on cardiac and aortic tissues using specific staining techniques to examine fibrosis and tunica media thickness.
Caspase-3 expression was measured immunohistochemically in aorta tissues.
Deltamethrin exposure was associated with increased cardiac damage and elevated serum ischemia-modified albumin and glucose levels.
Hesperidin treatment, especially at 300 mg/kg, significantly reduced ischemia-modified albumin and glucose levels compared to the DLM group.
Cardiac histopathological damage scores and tunica media thickness were significantly lower in the hesperidin-treated groups.
Caspase-3 expression was significantly reduced in the DLM + HSP group, indicating reduced apoptosis.

Abstract

Background and Objectives: Deltamethrin (DLM), a widely used pyrethroid insecticide, has been linked to cardiotoxic effects in non-target organisms. Hesperidin (HSP), a dietary bioflavonoid with antioxidant and cardioprotective properties, may counteract these effects. This study investigated the protective role of HSP against DLM-induced cardiotoxicity in male Wistar Albino rats. Materials and Methods: Thirty-two rats were divided into four groups: Control, DLM, DLM + HSP 100, and DLM + HSP 300. At the end of the experiment, serum ischemia-modified albumin (IMA), glucose, cholesterol, triglyceride, and HDL levels were analyzed. Cardiac and aortic tissues were assessed histopathologically. Masson’s trichrome staining evaluated cardiac fibrosis, Verhoeff–Van Gieson staining examined elastin and tunica media thickness, and caspase-3 expression in the aorta was determined immunohistochemically. Results: DLM administration caused cardiac and aortic damage by increasing IMA, glucose, caspase 3 activities, and tunica media thickness. HSP treatment, particularly at 300 mg/kg, reduced IMA (0.28 ± 0.02 vs. 0.60 ± 0.03 AU), glucose (141.12 ± 11.70 vs. 207.06 ± 9.85 mg/dL), cardiac histopathological damage score (2.17 ± 0.41 vs. 9.02 ± 1.35), tunica media thickness (95.29 ± 4.29 vs. 114.95 ± 17.20 µm), and caspase-3 expression score (0.62 ± 0.74 vs. 2.87 ± 0.35). All results showed significance at the p < 0.05 level. Conclusions: HSP exhibited dose-dependent protective effects against DLM-induced oxidative stress, apoptosis, and cardiovascular injury, suggesting its potential as a therapeutic candidate against pesticide-related cardiotoxicity.

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