salvianolic-acid-B and Cardiotoxicity

Doxorubicin (DOX)-induced cardiotoxicity is a clinically complex syndrome that leads to significant pain to cancer survivors. Endoplasmic reticulum (ER) stress has been suggested to be an important contributor to myocardium dysfunction during this phenomenon. Our previous study proved that Salvianolic acid B (Sal B) protected against doxorubicin induced cardiac dysfunction by inhibiting ER stress and cardiomyocyte apoptosis. However, the underlying molecular mechanism is not yet clearly. In this study, we investigated the protective effect and mechanisms of Sal B againest DOX-induced cardiac injury and ER stress in vivo and in vitro. After pretreatment with Sal B (0.25, 0.5, 1mg/kg i.v.) for 7 days, male SD rats were intraperitoneally injected with a single dose of DOX (3mg/kg) every 2 days for three injections. The cardioprotective effect of Sal B was observed 2 weeks after the first administration. Adult rat ventricular myocytes were isolated and treated with Sal B (20μg/ml) for 6h and then exposed in DOX (1μm) for 4h. The cardiomyocyte contractility and the level of intracellular Ca

Topics: Animals; Apoptosis; Benzofurans; Calcium Signaling; Cardiotoxicity; Cytoprotection; Disease Models, Animal; Dose-Response Relationship, Drug; Doxorubicin; Endoplasmic Reticulum; Endoplasmic Reticulum Stress; Heart Diseases; Male; Membrane Potential, Mitochondrial; Myocardial Contraction; Myocytes, Cardiac; Protective Agents; Rats, Sprague-Dawley; Time Factors; TRPC Cation Channels