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Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis

  • Authors:
    • Chenglei Su
    • Xinhui Fan
    • Feng Xu
    • Jiali Wang
    • Yuguo Chen
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    Affiliations: Department of Emergency Medicine, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China
    Copyright: © Su et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 110
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    Published online on: December 2, 2020
       https://doi.org/10.3892/mmr.2020.11749
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Abstract

Post‑cardiac arrest myocardial dysfunction (PAMD) is a leading cause of death in patients undergoing resuscitation patients following cardiac arrest (CA). Although prostaglandin E1 (PGE1) is a clinical drug used to mitigate ischemia injury, its effect on PAMD remains unknown. In the present study, the protective effects of PGE1 on PAMD were evaluated in a rat model of CA and in a hypoxia‑reoxygenation (H/R) in vitro model. Rats were randomly assigned to CA, CA+PGE1 or sham groups. Asphyxia for 8 min followed by cardiopulmonary resuscitation were performed in the CA and CA+PGE1 groups. PGE1 was intravenously administered at the onset of return of spontaneous circulation (ROSC). PGE1 treatment significantly increased the ejection fraction and cardiac output within 4 h following ROSC and improved the survival rate, compared with the CA group. Moreover, PGE1 inactivated GSK3β, prevented mitochondrial permeability transition pore (mPTP) opening, while reducing cytochrome c and cleaved caspase‑3 expression, as well as cardiomyocyte apoptosis in the rat model. To examine the underlying mechanism, H/R H9c2 cells were treated with PGE1 at the start of reoxygenation. The changes in GSK3β activity, mPTP opening, cytochrome c and cleaved caspase‑3 expression, and apoptosis of H9c2 cells were consistent with those noted in vivo. The results indicated that PGE1 attenuated PAMD by inhibiting mitochondria‑mediated cardiomyocyte apoptosis.
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Copy and paste a formatted citation
Spandidos Publications style
Su C, Fan X, Xu F, Wang J and Chen Y: Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis. Mol Med Rep 23: 110, 2021.
APA
Su, C., Fan, X., Xu, F., Wang, J., & Chen, Y. (2021). Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis. Molecular Medicine Reports, 23, 110. https://doi.org/10.3892/mmr.2020.11749
MLA
Su, C., Fan, X., Xu, F., Wang, J., Chen, Y."Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis". Molecular Medicine Reports 23.2 (2021): 110.
Chicago
Su, C., Fan, X., Xu, F., Wang, J., Chen, Y."Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis". Molecular Medicine Reports 23, no. 2 (2021): 110. https://doi.org/10.3892/mmr.2020.11749
Copy and paste a formatted citation
x
Spandidos Publications style
Su C, Fan X, Xu F, Wang J and Chen Y: Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis. Mol Med Rep 23: 110, 2021.
APA
Su, C., Fan, X., Xu, F., Wang, J., & Chen, Y. (2021). Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis. Molecular Medicine Reports, 23, 110. https://doi.org/10.3892/mmr.2020.11749
MLA
Su, C., Fan, X., Xu, F., Wang, J., Chen, Y."Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis". Molecular Medicine Reports 23.2 (2021): 110.
Chicago
Su, C., Fan, X., Xu, F., Wang, J., Chen, Y."Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis". Molecular Medicine Reports 23, no. 2 (2021): 110. https://doi.org/10.3892/mmr.2020.11749
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