Objective This study aimed to investigate the protective effects of dicoumarol on pathological cardiac hypertrophy induced by stress overload, thus providing scientific evidence for its potential therapeutic role. Methods We established pathological cardiac hypertrophy models in vitro using primary cardiomyocytes and in vivo using mice, administering dicoumarol and evaluating its protective effects against cardiac hypertrophy. Isoproterenol stimulation was employed to induce cardiomyocyte hypertrophy in the primary cell culture. The cells were categorized into control and treatment groups. Immunofluorescence staining was conducted after 24 hours of stimulation to evaluate cellular area. In the mouse model, pathological cardiac hypertrophy was induced via aortic constriction. Mice were divided into solvent control and treatment groups, with each group comprising 9 mice. The treatment group received dicoumarol at a dosage of 10 mg / kg every day. Four weeks post-surgery, cardiac structure and function were evaluated using echocardiography, while the degree of cardiac hypertrophy and fibrosis was  assessed via histopathological staining. Results In the in vitro model, dicoumarol significantly attenuated isoproterenol-induced cardiomyocyte hypertrophy.In the mouse model of myocardial hypertrophy, dicoumarol administration markedly ameliorated pressure overload-induced cardiac dysfunction, myocardial hypertrophy, and fibrosis compared to the solvent control group. Conclusion Dicoumarol exhibits protective effects against pressure overload-induced pathological myocardial hypertrophy and fibrosis, thereby improving cardiac function.

dicoumarol, myocardial hypertrophy, cardiac function