Epigallocatechin‑3‑gallate and zinc provide anti‑apoptotic protection against hypoxia/reoxygenation injury in H9c2 rat cardiac myoblast cells

Zeng,Xing; Tan,Xuerui

doi:10.3892/mmr.2015.3603

Epigallocatechin‑3‑gallate and zinc provide anti‑apoptotic protection against hypoxia/reoxygenation injury in H9c2 rat cardiac myoblast cells

Authors:
- Xing Zeng
- Xuerui Tan
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Affiliations: Department of Cardiology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, P.R. China
Published online on: April 8, 2015 https://doi.org/10.3892/mmr.2015.3603
Pages: 1850-1856
Copyright: © Zeng et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

It has previously been demonstrated that phosphatidylinositol‑3‑kinase (PI3K)/Akt and cleaved caspase‑3 serve critical roles in the apoptosis of cardiac myocytes following ischemia/reperfusion injury. Epigallocatechin‑3‑gallate (EGCG), the predominant catechin component of green tea, has been reported to have potential cardioprotective effects in primary cultures of cardiac myocytes exposed to I/R injury, mediated through inhibition of signal transducers and activators of transcription‑1 activity. In addition, it is also known that the biological behavior of EGCG may be influenced by metal ions, for example the hepatoprotective activity of EGCG has been reported to be enhanced by zinc. In the present study, the protective effects of EGCG with zinc were assessed on cultures of rat cardiac myoblasts exposed to hypoxia/reoxygenation (H/R) injury. H9c2 cells were subjected to 3‑h hypoxia, followed by 1‑h reperfusion. EGCG and/or zinc were perfused prior to induced hypoxic stress. It was demonstrated that when EGCG interacted with zinc, the anti‑apoptotic activity was significantly enhanced. To the best of our knowledge, the current study was the first to demonstrate that EGCG + Zn2+ protects H9c2 cells against H/R injury through activation of the PI3K/Akt pathway, as determined by western blotting. Since EGCG + Zn2+ may, at least in part, protect cardiac myocytes against H/R‑induced apoptotic cell death, the PI3K/Akt pathway of EGCG may be enhanced by its interactions with zinc during H/R injury. Furthermore, it was suggested that a similar procedure may be implemented in a clinical setting, in order to maximize PI3K/Akt activation levels in patients with acute coronary artery disease. EGCG and zinc may therefore represent effective agents for use in the prevention of I/R injury in clinical practice.

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