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Oxidative Medicine and Cellular Longevity
Volume 2012, Article ID 935738, 9 pages
http://dx.doi.org/10.1155/2012/935738
Research Article

Astragaloside IV Inhibits Oxidative Stress-Induced Mitochondrial Permeability Transition Pore Opening by Inactivating GSK-3 via Nitric Oxide in H9c2 Cardiac Cells

1Department of Internal Medicine, Hebei United University, Tangshan 063000, China
2Department of Physiology, Yanbian University, Yanji 133002, China
3Heart Institute, Hebei United University, Tangshan 063000, China
4Department of Anesthesiology, The University of North Carolina at Chapel Hill, CB No. 7010, Chapel Hill, NC 27599, USA

Received 19 June 2012; Accepted 13 August 2012

Academic Editor: Paola Venditti

Copyright © 2012 Yonggui He 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

Figure 1S shows the chemical structure of Astragaloside IV (C41H68O14, Molecular Weight 784.97). To confirm that the effect of astragaloside IV on TMRE fluorescence results from the inhibition of mPTP opening but not from mitochondrial uncoupling, the mitochondrial uncoupler FCCP was applied to test its effect on TMRE fluorescence. FCCP (0.5 µM) induced a marked decrease in TMRE fluorescence (45.09 ± 5.51% of baseline in the control group). Astragaloside IV did not change the TMRE fluorescence decrease caused by FCCP (Figure 2S). The GSK-3β inhibitor SB216763 (3 µM) and the specific mPTP inhibitor cyclosporin A (0.2 µM) could mimic the effect of astragaloside IV to prevent the loss of TMRE fluorescence, suggesting that astragaloside IV may protect the heart from reperfusion injury by modulating the mPTP opening (Figure 3S). Finally, Figure 4S shows the signaling mechanism responsible for the acrdioprotective effects of astragaloside IV.

  1. Supplementary Material