AMP-Activated Protein Kinase Activation during Cardioplegia-Induced Hypoxia/Reoxygenation Injury Attenuates Cardiomyocytic Apoptosis via Reduction of Endoplasmic Reticulum Stress

<table>Reverse transcription PCR analysis showed up-regulation of ATF6, VEGF, Grp78, and spliced XBP-1 mRNAs in HL-1 cardiomyocytes from different groups. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) served as the loading control. The PCR products of GAPDH, ATF6, VEGF, Grp78, and spliced XBP-1 were designed to be around 200 bp. Quantitative real-time PCR showed an elevated ratio of these mRNAs in various groups. (Results are representative of at least 3 separate experiments. *<svg height="10.1" id="M8" style="vertical-align:-0.27pt" version="1.1" viewbox="0 0 43.337502 10.1" width="43.337502" xmlns="http://www.w3.org/2000/svg">
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Mediators of Inflammation

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Figure 3

Figure 3: AMP-Activated Protein Kinase Activation during Cardioplegia-Induced Hypoxia/Reoxygenation Injury Attenuates Cardiomyocytic Apoptosis via Reduction of Endoplasmic Reticulum Stress 

Figure 3 | AMP-Activated Protein Kinase Activation during Cardioplegia-Induced Hypoxia/Reoxygenation Injury Attenuates Cardiomyocytic Apoptosis via Reduction of Endoplasmic Reticulum Stress 