TY - JOUR AB - Arsenic trioxide (ATO) is a frontline chemotherapy drug used in the therapy of acute promyelocytic leukemia. However, the clinical use of ATO is hindered by its cardiotoxicity. The present study aimed to observe the potential effects and underlying mechanisms of tannic acid (TA) against ATO‑induced cardiotoxicity. Male rats were intraperitoneally injected with ATO (5 mg/kg/day) to induce cardiotoxicity. TA (20 and 40 mg/kg/day) was administered to evaluate its cardioprotective efficacy against ATO‑induced heart injury in rats. Administration of ATO resulted in pathological damage in the heart and increased oxidative stress as well as levels of serum cardiac biomarkers creatine kinase and lactate dehydrogenase and the inflammatory marker NF‑κB (p65). Conversely, TA markedly reversed this phenomenon. Additionally, TA treatment caused a notable decrease in the expression levels of cleaved caspase‑3/caspase‑3, Bax, p53 and Bad, while increasing Bcl‑2 expression levels. Notably, the application of TA decreased the expression levels of cytochrome c, second mitochondria‑derived activator of caspases and high‑temperature requirement A2, which are apoptosis mitochondrial‑associated proteins. The present findings indicated that TA protected against ATO‑induced cardiotoxicity, which may be associated with oxidative stress, inflammation and mitochondrial apoptosis. AD - School of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang, Hebei 050200, P.R. China School of Basic Medicine, Hebei University of Chinese Medicine, Shijiazhuang, Hebei 050200, P.R. China The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China AU - Xue,Yucong AU - Li,Mengying AU - Xue,Yurun AU - Jin,Weiyue AU - Han,Xue AU - Zhang,Jianping AU - Chu,Xi AU - Li,Ziliang AU - Chu,Li DA - 2020/12/01 DO - 10.3892/mmr.2020.11586 EP - 4674 IS - 6 JO - Mol Med Rep KW - arsenic trioxide cardiotoxicity tannic acid oxidative stress mitochondrial apoptosis PY - 2020 SN - 1791-2997 1791-3004 SP - 4663 ST - Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis T2 - Molecular Medicine Reports TI - Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis UR - https://doi.org/10.3892/mmr.2020.11586 VL - 22 ER -