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. 2020 Aug 27;8:833. doi: 10.3389/fcell.2020.00833

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Copyright © 2020 Deng, Chen, Zhang, Li, He and Tan.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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AMPK2α overexpression attenuates hypoxia/reoxygenation-mediated cardiomyocyte dysfunction and apoptosis. Adenovirus loaded with AMPKα2 were transfected into cardiomyocytes before H/R injury. (A) H/R injury was established through 1-h hypoxia, 2-h reoxygenation RNA was isolated from cardiomyocyte, and qPCR was used to evaluate the transcription of AMPKα2. (B) Proteins were collected from H/R-treated cardiomyocytes, and then, the expression of AMPKα2 was determined through western blots. (C) MTT assay was used to evaluate cell viability in response to H/R injury. (D,E) ELISA assay was used to measure the levels of troponin T (TnT) and creatine kinase-MB (CK-MB) in H/R-treated cardiomyocytes. (F–H) The cardiomyocytes contractile properties in the context of HI/R injury. The data represent the mean ± SEM. P < 0.05.