Research Journal of Chemistry

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Cardioprotective Effects of Peonidin against Doxorubicin-induced Cardiotoxicity in Wistar Rats: Electrophysiological, Biochemical and Histopathological Evaluation

Jyothirmai Namathoti and Rajeshwari Pasupula

Res. J. Chem. Environ.; Vol. 29(8); 80-86; doi: https://doi.org/10.25303/298rjce080086; (2025)

Abstract
Doxorubicin (DOX) is a widely used chemotherapeutic agent known for its potent anticancer effects; however, its clinical utility is limited due to severe cardiotoxicity. The present study investigates the cardioprotective potential of peonidin against DOX-induced myocardial injury in Wistar rats. Wistar rats (155-180 g) were divided into four groups such as normal control with no treatment, DOX treatment, DOX with 200 mg/kg of peonidin and DOX with 400 mg/kg of peonidin administered subcutaneously (15 mg/kg) on the 8th and 9th days to induce cardiotoxicity. Peonidin was orally administered for seven days before DOX treatment. Blood samples were collected for biochemical analysis and histopathological and electrophysiological assessments were performed to evaluate myocardial damage and inflammation. DOX administration results in significant cardiac dysfunction, as evidenced by prolonged ST interval, decreased R wave amplitude, increased left ventricular end-diastolic pressure (LVEDP) and decreased left ventricular systolic pressure (LVSP).

Elevated levels of cardiac biomarkers (LDH, CK and troponin) and inflammatory mediators (IL-6 and TNF-α) further confirm myocardial injury. Peonidin pre-treatment demonstrates a dose-dependent cardioprotective effect, with the 400 mg/kg dose showing significant improvements in ST interval, R wave amplitude, LVSP and ± dp/dtmax. Biochemical analysis reveals a substantial reduction in LDH, CK and troponin levels in the 400 mg/kg group. Histopathological examination further confirms reduced necrosis and preserved myocardial integrity in peonidin-treated rats. It was concluded that peonidin exhibits potent cardioprotective effects against DOX-induced myocardial injury through antioxidative, anti-inflammatory and membrane-stabilizing mechanisms.