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Journal of Diabetes Research
Volume 2016 (2016), Article ID 1390861, 8 pages
Research Article

ALDH2 Inhibition Potentiates High Glucose Stress-Induced Injury in Cultured Cardiomyocytes

1Division of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Health System, Detroit, MI 48202, USA
2Department of Cardiovascular Sciences, Center for Cardiovascular Regeneration, Houston Methodist Research Institute, Houston, TX, USA
3Department of Physiology, Wayne State University, Detroit, MI 48202, USA

Received 20 April 2016; Revised 26 July 2016; Accepted 22 August 2016

Academic Editor: Kim Connelly

Copyright © 2016 Guodong Pan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

Supplementary Figure  1: Dose-response curve of disulfiram with ALDH2 activity in H9c2 cells. H9c2 cells were exposed to difference concentration of DSF (0–10 μM) over night. The inhibition of ALDH2 activity presents a DSF dose-dependent manner. Supplementary Figure  2: ALDH2 inhibition by pretreating with disulfiram (DSF) and superoxide levels in mitochondria. (a) Representative photomicrographs of MitoSOX staining from each treatment groups. The red fluoresce indicates superoxide in mitochondria. (b) Increase superoxide in mitochondria in cultured H9C2 cardiomyocytes subjected to high glucose stress (G2) compared to equimolar mannitol (G1). Disulfiram (DSF) pretreatment increased ROS levels in both mannitol (G3) and high glucose (G4) groups. The data expressed are mean ± SEM. N = 4–6. p<0.05 versus G1, p#<0.05 versus G2, and p$<0.05 versus G3.

  1. Supplementary Material