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Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

  • Authors:
    • Yucong Xue
    • Mengying Li
    • Yurun Xue
    • Weiyue Jin
    • Xue Han
    • Jianping Zhang
    • Xi Chu
    • Ziliang Li
    • Li Chu
  • View Affiliations / Copyright

    Affiliations: 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
    Copyright: © Xue et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 4663-4674
    |
    Published online on: October 11, 2020
       https://doi.org/10.3892/mmr.2020.11586
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Abstract

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.
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Copy and paste a formatted citation
Spandidos Publications style
Xue Y, Li M, Xue Y, Jin W, Han X, Zhang J, Chu X, Li Z and Chu L: Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis. Mol Med Rep 22: 4663-4674, 2020.
APA
Xue, Y., Li, M., Xue, Y., Jin, W., Han, X., Zhang, J. ... Chu, L. (2020). Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis. Molecular Medicine Reports, 22, 4663-4674. https://doi.org/10.3892/mmr.2020.11586
MLA
Xue, Y., Li, M., Xue, Y., Jin, W., Han, X., Zhang, J., Chu, X., Li, Z., Chu, L."Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis". Molecular Medicine Reports 22.6 (2020): 4663-4674.
Chicago
Xue, Y., Li, M., Xue, Y., Jin, W., Han, X., Zhang, J., Chu, X., Li, Z., Chu, L."Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis". Molecular Medicine Reports 22, no. 6 (2020): 4663-4674. https://doi.org/10.3892/mmr.2020.11586
Copy and paste a formatted citation
x
Spandidos Publications style
Xue Y, Li M, Xue Y, Jin W, Han X, Zhang J, Chu X, Li Z and Chu L: Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis. Mol Med Rep 22: 4663-4674, 2020.
APA
Xue, Y., Li, M., Xue, Y., Jin, W., Han, X., Zhang, J. ... Chu, L. (2020). Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis. Molecular Medicine Reports, 22, 4663-4674. https://doi.org/10.3892/mmr.2020.11586
MLA
Xue, Y., Li, M., Xue, Y., Jin, W., Han, X., Zhang, J., Chu, X., Li, Z., Chu, L."Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis". Molecular Medicine Reports 22.6 (2020): 4663-4674.
Chicago
Xue, Y., Li, M., Xue, Y., Jin, W., Han, X., Zhang, J., Chu, X., Li, Z., Chu, L."Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis". Molecular Medicine Reports 22, no. 6 (2020): 4663-4674. https://doi.org/10.3892/mmr.2020.11586
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