Cardioprotective potential of Rosuvastatin against isoproterenol induced cardiac dysfunction and hypertrophy in the experimental model of rodents

Aims

Cardiovascular disease is the primary cause of mortality and morbidity, and its terminal phase is chronic heart failure. The present study aimed to examine the protective impact of rosuvastatin on isoproterenol-induced chronic heart failure and investigate plausible related mechanisms. Rosuvastatin, a drug with multiple pleiotropic properties, has been examined for its cardioprotective effects in heart failure induced by isoproterenol.

Methods

Male Sprague Dawley rats were given isoproterenol 5 ​mg/kg once a day for 7 days to establish heart failure by subcutaneous injection. Simultaneously, rosuvastatin (10 ​mg/kg) was orally administrated from day 1 to day 14. Protective effects were evaluated by heart grading and gross morphology, hemodynamic parameter, cardiac troponin I, heart mitochondrial enzyme and lysosomal hydrolases and pro inflammatory cytokines levels were analyzed.

Results

Rosuvastatin (10 ​mg/kg) significantly attenuated isoproterenol-induced hypertrophy, remodeling and dysfunction of the ventricle, reduced the heart mitochondrial enzyme and lysosomal hydrolases and normalized the increased hemodynamic and pro inflammatory cytokines levels.

Conclusions

The study highlights the preventive effects of, rosuvastatin, against heart failure. The results of the research indicate that rosuvastatin has cardioprotective effects on the experimental model, which were supported by several characteristics. However, further research is required to identify the precise molecular mechanisms and signalling pathways of rosuvastatin's impact on heart failure.