Tanshinone‑IIA inhibits myocardial infarct via decreasing of the mitochondrial apoptotic signaling pathway in myocardiocytes

production, decreased ATF4 and IRE1α expression, and reduced intracellular calcium and oxidative stress in myocardiocytes. Furthermore, caspase‑3 overexpression blocked Tan‑IIA‑decreased apoptosis of myocardiocytes. In conclusion, the data in the present study indicated that Tan‑IIA improved myocardial infarct and apoptosis via the endoplasmic reticulum stress‑dependent pathway and mitochondrial apoptotic signaling pathway.