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Article

Eriodictyol protects H9c2 cardiomyocytes against the injury induced by hypoxia/reoxygenation by improving the dysfunction of mitochondria

  • Authors:
    • Yanli Xie
    • Rongwei Ji
    • Minghui Han
  • View Affiliations / Copyright

    Affiliations: Department of Cardiothoracic Surgery, Wuhan Women and Children Medical Care Center, Wuhan, Hubei 430000, P.R. China, Department of Pathology, Xi'an XD Group Hospital, Xi'an, Shaanxi 710077, P.R. China, Department of Thoracic Surgery, The First People's Hospital of Qingdao Economic and Technological Development Zone, Qingdao, Shandong 266555, P.R. China
  • Pages: 551-557
    |
    Published online on: November 2, 2018
       https://doi.org/10.3892/etm.2018.6918
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Abstract

Myocardial infarction is a leading cause of mortality worldwide, while myocardial ischemia and timely reperfusion contribute to myocardial injury. The mitochondria are involved in the injury and mediate the apoptosis of cardiomyocytes. In order to develop novel therapeutic approaches for myocardial infarction, the present study evaluated the myocardial protective effects of eriodictyol and investigated relevant mechanisms in H9c2 cardiomyocytes. As a result, eriodictyol was observed to improve the H9c2 cardiomyocyte viability and block the leakage of cytosolic lactate dehydrogenase under hypoxia/reoxygenation. In addition, the dysfunction of mitochondria induced by hypoxia/reoxygenation was ameliorated by eriodictyol through suppressing the overload of intracellular Ca2+, preventing overproduction of reactive oxygen species, blocking mitochondrial permeability transition pore opening, increasing mitochondrial membrane potential level and decreasing ATP depletion. Finally, the apoptosis of H9c2 cardiomyocyte induced by hypoxia/reoxygenation was prevented by eriodictyol through upregulation of the expression of B‑cell lymphoma‑2 (Bcl‑2) and downregulation of the expression levels of Bcl‑2‑associated X protein and caspase‑3. These results provided evidence for further investigation on myocardial protection and the treatment of myocardial infarction using eriodictyol.
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Copy and paste a formatted citation
Spandidos Publications style
Xie Y, Ji R and Han M: Eriodictyol protects H9c2 cardiomyocytes against the injury induced by hypoxia/reoxygenation by improving the dysfunction of mitochondria. Exp Ther Med 17: 551-557, 2019.
APA
Xie, Y., Ji, R., & Han, M. (2019). Eriodictyol protects H9c2 cardiomyocytes against the injury induced by hypoxia/reoxygenation by improving the dysfunction of mitochondria. Experimental and Therapeutic Medicine, 17, 551-557. https://doi.org/10.3892/etm.2018.6918
MLA
Xie, Y., Ji, R., Han, M."Eriodictyol protects H9c2 cardiomyocytes against the injury induced by hypoxia/reoxygenation by improving the dysfunction of mitochondria". Experimental and Therapeutic Medicine 17.1 (2019): 551-557.
Chicago
Xie, Y., Ji, R., Han, M."Eriodictyol protects H9c2 cardiomyocytes against the injury induced by hypoxia/reoxygenation by improving the dysfunction of mitochondria". Experimental and Therapeutic Medicine 17, no. 1 (2019): 551-557. https://doi.org/10.3892/etm.2018.6918
Copy and paste a formatted citation
x
Spandidos Publications style
Xie Y, Ji R and Han M: Eriodictyol protects H9c2 cardiomyocytes against the injury induced by hypoxia/reoxygenation by improving the dysfunction of mitochondria. Exp Ther Med 17: 551-557, 2019.
APA
Xie, Y., Ji, R., & Han, M. (2019). Eriodictyol protects H9c2 cardiomyocytes against the injury induced by hypoxia/reoxygenation by improving the dysfunction of mitochondria. Experimental and Therapeutic Medicine, 17, 551-557. https://doi.org/10.3892/etm.2018.6918
MLA
Xie, Y., Ji, R., Han, M."Eriodictyol protects H9c2 cardiomyocytes against the injury induced by hypoxia/reoxygenation by improving the dysfunction of mitochondria". Experimental and Therapeutic Medicine 17.1 (2019): 551-557.
Chicago
Xie, Y., Ji, R., Han, M."Eriodictyol protects H9c2 cardiomyocytes against the injury induced by hypoxia/reoxygenation by improving the dysfunction of mitochondria". Experimental and Therapeutic Medicine 17, no. 1 (2019): 551-557. https://doi.org/10.3892/etm.2018.6918
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