Open Access

Attenuation of doxorubicin-induced cardiotoxicity by esculetin through modulation of Bmi-1 expression

  • Authors:
    • Fan Xu
    • Xiao Li
    • Lanfang Liu
    • Xu Xiao
    • Li Zhang
    • Shenglin Zhang
    • Pingping Lin
    • Xiaojie Wang
    • Yongwei Wang
    • Qingshan Li
  • View Affiliations

  • Published online on: July 10, 2017     https://doi.org/10.3892/etm.2017.4763
  • Pages: 2216-2220
  • Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The protective effects and mechanisms of esculetin on doxorubicin (DOX)-induced injury of H9c2 cells were investigated. H9c2 cells were cultured and the logarithmic growth phase of the cells was divided into a control group, a DOX group and an esculetin + DOX group. Cell viability was detected by MTT assay. Annexin V-PI (AV-PI) double staining flow cytometry was carried out to detect cell apoptosis. Intracellular reactive oxygen species (ROS) were detected by flow cytometry. Transmission electron microscope (TEM) was used to evaluate cell ultrastructure. Cleaved caspase-3, cleaved PARP, Bcl-2, Bid and Bmi-1 proteins levels were investigated by western blot analysis. Bmi-1 siRNA was used to detect the role of Bmi-1 in the protective effects of esculetin against DOX-induced toxicity in H9c2 cells. The MTT and AV-PI double staining results showed that esculetin significantly increased H9c2 cell viability. Compared with the control group, the levels of cleaved caspase-3, cleaved PARP, Bid and ROS levels were significantly decreased, but the expression of Bcl-2 and Bmi-1 were significantly increased in the esculetin + DOX group. TEM showed that the cell structure of the mitochondria was protected by esculetin. The results of Bmi-1 siRNA showed that esculetin could protect DOX-induced cardiotoxicity by modulating Bmi-1 expression. Esculetin can protect DOX-induced cardiotoxicity and the effects may be attributable to modulation of Bmi-1 expression, provoking intracellular ROS accumulation, protecting the structure of mitochondria and reducing cell apoptosis.

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September-2017
Volume 14 Issue 3

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Copy and paste a formatted citation
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Spandidos Publications style
Xu F, Li X, Liu L, Xiao X, Zhang L, Zhang S, Lin P, Wang X, Wang Y, Li Q, Li Q, et al: Attenuation of doxorubicin-induced cardiotoxicity by esculetin through modulation of Bmi-1 expression. Exp Ther Med 14: 2216-2220, 2017
APA
Xu, F., Li, X., Liu, L., Xiao, X., Zhang, L., Zhang, S. ... Li, Q. (2017). Attenuation of doxorubicin-induced cardiotoxicity by esculetin through modulation of Bmi-1 expression. Experimental and Therapeutic Medicine, 14, 2216-2220. https://doi.org/10.3892/etm.2017.4763
MLA
Xu, F., Li, X., Liu, L., Xiao, X., Zhang, L., Zhang, S., Lin, P., Wang, X., Wang, Y., Li, Q."Attenuation of doxorubicin-induced cardiotoxicity by esculetin through modulation of Bmi-1 expression". Experimental and Therapeutic Medicine 14.3 (2017): 2216-2220.
Chicago
Xu, F., Li, X., Liu, L., Xiao, X., Zhang, L., Zhang, S., Lin, P., Wang, X., Wang, Y., Li, Q."Attenuation of doxorubicin-induced cardiotoxicity by esculetin through modulation of Bmi-1 expression". Experimental and Therapeutic Medicine 14, no. 3 (2017): 2216-2220. https://doi.org/10.3892/etm.2017.4763