文献类型：期刊文献

英文题名：Tanshinone IIA Accomplished Protection against Radiation-Induced Cardiomyocyte Injury by Regulating the p38/p53 Pathway

作者：Wang, Gang[1];Ma, Li[2];Wang, Bowen[3];Gao, Fentang[3];Li, Jianfeng[3];Cai, Hongyi[4];Wang, Juan[3];Zhang, Tiancheng[3];Guo, Hao[5];Xie, Ping[3];Li, Yi[6]

第一作者：王钢

通信作者：Xie, P[1];Li, Y[2]

机构：[1]Gansu Univ Chinese Med, Clin Med Coll 1, Lanzhou 730000, Peoples R China;[2]Gansu Prov Matern & Child Care Hosp, Lanzhou 730000, Peoples R China;[3]Gansu Prov Hosp, Dept Cardiovasc Med, Lanzhou 730000, Peoples R China;[4]Gansu Prov Hosp, Dept Radiotherapy, Lanzhou 730000, Peoples R China;[5]Xiamen Univ, Sch Med, Xiamen 361000, Peoples R China;[6]Lanzhou Univ, Sch Stomatol, Lanzhou 730000, Peoples R China

第一机构：甘肃中医药大学

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

年份：2022

卷号：2022

外文期刊名：MEDIATORS OF INFLAMMATION

收录：;Scopus(收录号：2-s2.0-85137014025);WOS:【SCI-EXPANDED(收录号:WOS:000855013500002)】；

基金：AcknowledgmentsA grant from the National Natural Science Foundation of China (No. 81860047) supported this study.

语种：英文

摘要：Background. Radiotherapy is one of the major strategies for treating tumors, and it inevitably causes damage to relevant tissues and organs during treatment. Radiation-induced heart disease (RIHD) refers to radiation-induced cardiovascular adverse effects caused by thoracic radiotherapy. Currently, there is no uniform standard in the treatment of RIHD. Methods. In our group study, by administering a dose of 4 Gy radiation, we established a radiation injured cardiomyocyte model and explored the regulatory relationship between tanshinone IIA and p38 MAPK in cardiomyocyte injury. We assessed cell damage and proliferation using clonogenic assay and lactate dehydrogenase (LDH) release assay. The measures of antioxidant activity and oxidative stress were conducted using superoxide dismutase (SOD) and reactive oxygen species (ROS). The apoptosis rate and the relative expression of apoptotic proteins were conducted using flow cytometry and western blot. To assess p38 and p53 expressions and phosphorylation levels, western blot was performed. Results. Experimental results suggested that tanshinone IIA restored cell proliferation in radiation-induced cardiomyocyte injury (**P < 0.01), and the level of LDH release decreased (*P < 0.05). Meanwhile, tanshinone IIA could decrease the ROS generation induced by radiation (**P < 0.01) and upregulate the SOD level (**P < 0.01). Again, tanshinone IIA reduced radiation-induced cardiomyocyte apoptosis (**P < 0.01). Finally, tanshinone IIA downregulated radiation-induced p38/p53 overexpression (***P < 0.001). Conclusions. The treatment effects of tanshinone IIA against radiation-induced myocardial injury may be through the regulation of the p38/p53 pathway.