文献类型：期刊文献

英文题名：Sodium Tanshinone IIA Sulfonate Prevents Radiation-Induced Toxicity in H9c2 Cardiomyocytes

作者：Zhang, Wenjing[1];Li, Yi[2,3];Li, Rui[4];Wang, Yaya[5];Zhu, Mengwen[4];Wang, Bowen[6];Li, Yanling[6];Li, Dongyun[7];Xie, Ping[6];Liu, Bin[4]

第一作者：张雯娟

通信作者：Liu, B[1];Xie, P[2]

机构：[1]Gansu Univ Tradit Chinese Med, Sch Clin Med, Lanzhou 730000, Gansu, Peoples R China;[2]Lanzhou Univ, Sch Basic Med Sci, Inst Med Genet, Lanzhou 730000, Peoples R China;[3]Gansu Cardiovasc Inst, Lanzhou 730050, Peoples R China;[4]Lanzhou Univ, Sch Stomatol, Lanzhou 730000, Gansu, Peoples R China;[5]Ningxia Med Univ, Sch Clin Med, Yinchuan 750000, Ningxia Hui Aut, Peoples R China;[6]Gansu Prov Hosp Lanzhou, Dept Cardiol, Lanzhou 730000, Gansu, Peoples R China;[7]Gansu Prov Hosp, Dept Radiol, Lanzhou 730000, Peoples R China

第一机构：甘肃中医药大学临床医学院

通信机构：[1]corresponding author), Lanzhou Univ, Sch Stomatol, Lanzhou 730000, Gansu, Peoples R China;[2]corresponding author), Gansu Prov Hosp Lanzhou, Dept Cardiol, Lanzhou 730000, Gansu, Peoples R China.

年份：2017

卷号：2017

外文期刊名：EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE

收录：;Scopus(收录号：2-s2.0-85016569732);WOS:【SCI-EXPANDED(收录号:WOS:000398499000001)】；

基金：This work was financially supported by the Cardiovascular Institute of Gansu Provincial Hospital and the School of Stomatology of Lanzhou University.

语种：英文

摘要：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 fromX-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.