Doxorubicin is a broad-spectrum antitumor chemotherapeutic drug. Due to its non-selective mechanism of action, it exhibits significant cardiotoxicity. Intravenous administration can cause dose-dependent, irreversible chronic myocardial injury and heart failure within hours or days. The mechanism of its myocardial toxicity may involve free radical release, mitochondrial damage, and metabolic imbalance, among others. This method is suitable for establishing acute heart failure models. It is simple and feasible, with a predictable onset of heart failure in a dose-dependent manner. High-dose short-term intraperitoneal administration results in high animal mortality and low modeling success rate; therefore, multiple low-dose intraperitoneal injections are commonly adopted. Heart failure induced by doxorubicin is characterized by biventricular dilation, thinning of ventricular walls, and reduced ejection fraction. This model is generally used to study the pathogenesis of cardiomyopathy and heart failure, as well as to evaluate novel therapeutic strategies.

Wistar rats (male, approximately 300 g)
Modeling method: Doxorubicin was dissolved in sterile saline solution and administered intraperitoneally once every 3 days for a total of 5 injections within 2 weeks, to successfully establish the heart failure model.

Positive drug: Captopril

Evaluation indicators: gross observation, HE staining, TUNEL staining, serum ELISA

gross observation

Serum ELISA

HE staining of myocardial tissue

TUNEL staining of myocardial tissue