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Evidence-Based Complementary and Alternative Medicine
Volume 2017 (2017), Article ID 4537974, 13 pages
Research Article

Sodium Tanshinone IIA Sulfonate Prevents Radiation-Induced Toxicity in H9c2 Cardiomyocytes

1School of Clinical Medicine, Gansu University of Traditional Chinese Medicine, Lanzhou, Gansu 730000, China
2The Institute of Medical Genetics, School of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, China
3Gansu Cardiovascular Institute, Lanzhou 730050, China
4School of Stomatology, Lanzhou University, Lanzhou, Gansu 730000, China
5School of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region 750000, China
6Department of Cardiology, Gansu Provincial Hospital, Lanzhou, Gansu 730000, China
7Radiology Department, Gansu Provincial Hospital, Lanzhou, Gansu 730000, China

Correspondence should be addressed to Ping Xie and Bin Liu

Received 10 August 2016; Revised 11 January 2017; Accepted 19 January 2017; Published 12 March 2017

Academic Editor: Raffaele Capasso

Copyright © 2017 Wenjing Zhang 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.


The present study was designed to elucidate the key parameters associated with X-ray radiation induced oxidative stress and the effects of STS on X-ray-induced toxicity in H9c2 cardiomyocytes. Cytotoxicity of STS and radiation was assessed by MTT. Antioxidant activity was evaluated by SOD and MDA. Apoptosis was measured by the flow cytometry, Hoechst 33258, clonogenic survival assay, and western blot. It was found that the cell viability of H9c2 cells exposed to X-ray radiation was significantly decreased in a dose-dependent manner and was associated with cell cycle arrest at the G0/G1 phase as well as apoptosis. STS treatment significantly reversed the morphological changes, attenuated radiation-induced apoptosis, and improved the antioxidant activity in the H9c2 cells. STS significantly increased the Bcl-2 and Bcl-2/Bax levels and decreased the Bax and caspase-3 levels, compared with the cells treated with radiation alone. STS treatment also resulted in a significant increase in p38-MAPK activation. STS could protect the cells from X-ray-induced cell cycle arrest, oxidative stress, and apoptosis. Therefore, we suggest the STS could be useful for the treatment of radiation-induced cardiovascular injury.