Arsenic trioxide (ATO) has been verified as a breakthrough with respect to the management\nof acute promyelocytic leukemia (APL) in recent decades but associated with some serious adverse\nphenomena, particularly cardiac functional abnormalities. Salvianolic acid A (Sal A) is a major\neffective component in treating ATO-induced cardiotoxicity. Therefore, the objective of our study\nwas to assess whether Sal A had protective effects by the regulation of calcium homeostasis and\nendoplasmic reticulum (ER) stress. For the in vivo study, BALB/c mice were treated with ATO\nand/or Sal A via daily tail vein injections for two weeks. For the in vitro study, we detected the effects\nof ATO and/or Sal A in real time using adult rat ventricular myocytes (ARVMs) and an IonOptix\nMyoCam system Our results showed that Sal A pretreatment alleviated cardiac dysfunction and\nCa2+ overload induced by ATO in vivo and vitro. Moreover, Sal A increased sarcoplasmic reticulum\n(SR) Ca2+-ATPase (SERCA) activity and expression, alleviated [Ca2+]ER depletion, and decreased\nER stress-related protein expression. Sal A protects the heart from ATO-induced injury and its\nadministration correlates with the modulation of SERCA, the recovery of Ca2+ homeostasis, and the\ndown-regulation of ER stress-mediated apoptosis
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