Open Access

(‑)‑Epicatechin protects against myocardial ischemia‑induced cardiac injury via activation of the PTEN/PI3K/AKT pathway

  • Authors:
    • Jia‑Wen Li
    • Xiao‑Yun Wang
    • Xin Zhang
    • Lei Gao
    • Li‑Feng Wang
    • Xin‑Hua Yin
  • View Affiliations

  • Published online on: April 12, 2018     https://doi.org/10.3892/mmr.2018.8870
  • Pages: 8300-8308
  • Copyright: © Li 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

Flavonol (‑)‑epicatechin (EPI) is primarily contained in green tea (Camellia sinensis) and cocoa beans (Theobroma cacao), and has been demonstrated to be beneficial for the health of the cardiovascular system. However, the effect and the underlying mechanism of EPI on myocardial ischemia induced cardiac injury has not yet been determined. Therefore, the present study aimed to detect whether EPI inhibited myocardial ischemia injury. An in vivo mouse myocardial ischemia model was induced by the ligation of left descending coronary artery for 7 days. EPI (1 mg/kg/day) was administrated 10 days prior to myocardial ischemia operation. The in vitro mouse myocardial ischemia model was induced by cultivating neonatal mouse cardiomyocytes under anoxia condition for 12 h. Cardiomyocytes were treated with EPI (5 µM) for 1 h and then incubated under anoxia conditions. Mouse hearts and cultured cardiomyocytes were used for hematoxylin‑eosin, masson, ultrasonography, terminal dUTP nick end‑labeling, immunofluorescence, western blotting and MTT assays. Results revealed that myocardial ischemia‑induced mouse cardiac injury was significantly inhibited by EPI, as evidenced by decreased myocardial apoptosis, cardiac fibrosis and myocardial hypertrophy and improved cardiac function. In addition, it was confirmed that EPI serves a protective effect against myocardial ischemia via the phosphatase and tensin homolog (PTEN)/phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling pathway, which was reversed by the PI3K inhibitor, LY294002. The protective role of EPI in myocardial apoptosis was further confirmed on mouse cardiomyocytes following anoxia treatment in vitro. In conclusion, the data suggested that EPI protects against myocardial ischemia induced cardiac injury through the PTEN/PI3K/AKT signaling pathway in vivo and in vitro, which may provide clinical therapeutic approaches and targets for cardiac ischemia injury.
View Figures
View References

Related Articles

Journal Cover

June-2018
Volume 17 Issue 6

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Li JW, Wang XY, Zhang X, Gao L, Wang LF and Yin XH: (‑)‑Epicatechin protects against myocardial ischemia‑induced cardiac injury via activation of the PTEN/PI3K/AKT pathway. Mol Med Rep 17: 8300-8308, 2018.
APA
Li, J., Wang, X., Zhang, X., Gao, L., Wang, L., & Yin, X. (2018). (‑)‑Epicatechin protects against myocardial ischemia‑induced cardiac injury via activation of the PTEN/PI3K/AKT pathway. Molecular Medicine Reports, 17, 8300-8308. https://doi.org/10.3892/mmr.2018.8870
MLA
Li, J., Wang, X., Zhang, X., Gao, L., Wang, L., Yin, X."(‑)‑Epicatechin protects against myocardial ischemia‑induced cardiac injury via activation of the PTEN/PI3K/AKT pathway". Molecular Medicine Reports 17.6 (2018): 8300-8308.
Chicago
Li, J., Wang, X., Zhang, X., Gao, L., Wang, L., Yin, X."(‑)‑Epicatechin protects against myocardial ischemia‑induced cardiac injury via activation of the PTEN/PI3K/AKT pathway". Molecular Medicine Reports 17, no. 6 (2018): 8300-8308. https://doi.org/10.3892/mmr.2018.8870