Open Access

Peptide Szeto‑Schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway

  • Authors:
    • Li Zhang
    • Mengwen Feng
    • Xuejun Wang
    • Hao Zhang
    • Jingjing Ding
    • Zijie Cheng
    • Lingmei Qian
  • View Affiliations

  • Published online on: February 25, 2021     https://doi.org/10.3892/ijmm.2021.4896
  • Article Number: 63
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Oxidative stress serves a key role in doxorubicin (DOX)‑induced cardiotoxicity. The peptide Szeto‑Schiller (SS)31 is an efficacious antioxidant with the capacity to reduce mitochondrial reactive oxygen species (ROS) levels and scavenge free radicals. Although SS31 is involved in the pathophysiological process of various cardiovascular diseases, the role of SS31 in DOX‑induced cardiotoxicity remains unclear. To explore the effects of SS31 in DOX‑induced cardiotoxicity, the present study first constructed DOX‑induced cardiotoxicity models, in which H9c2 cells were incubated with 1 µM DOX for 24 h and C57BL/6 mice were administered DOX (20 mg/kg cumulative dose). The results of various assays in these models demonstrated that SS31 exhibited a cardioprotective effect in vitro and in vivo by attenuating the level of ROS, stabilizing the mitochondrial membrane potential and ameliorating myocardial apoptosis as well as fibrosis following treatment with DOX. Mechanistically, the results of the present study revealed that the p38 MAPK signaling pathway was inhibited by SS31 in DOX‑treated H9c2 cells, which was associated with the cardioprotective function of SS31. In addition, P79350, a selective agonist of p38 MAPK, reversed the protective effects of SS31. Taken together, these results demonstrated the effects of SS31 on ameliorating DOX‑induced cardiotoxicity and indicated its potential as a drug for the treatment of DOX‑induced cardiotoxicity.
View Figures
View References

Related Articles

Journal Cover

April-2021
Volume 47 Issue 4

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Zhang L, Feng M, Wang X, Zhang H, Ding J, Cheng Z and Qian L: Peptide Szeto‑Schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway. Int J Mol Med 47: 63, 2021.
APA
Zhang, L., Feng, M., Wang, X., Zhang, H., Ding, J., Cheng, Z., & Qian, L. (2021). Peptide Szeto‑Schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway. International Journal of Molecular Medicine, 47, 63. https://doi.org/10.3892/ijmm.2021.4896
MLA
Zhang, L., Feng, M., Wang, X., Zhang, H., Ding, J., Cheng, Z., Qian, L."Peptide Szeto‑Schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway". International Journal of Molecular Medicine 47.4 (2021): 63.
Chicago
Zhang, L., Feng, M., Wang, X., Zhang, H., Ding, J., Cheng, Z., Qian, L."Peptide Szeto‑Schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway". International Journal of Molecular Medicine 47, no. 4 (2021): 63. https://doi.org/10.3892/ijmm.2021.4896