文献类型：期刊文献

英文题名：Astragalus Polysaccharide Eases G1 Phase-Correlative Bystander Effects through Mediation of TGF-beta R/MAPK/ROS Signal Pathway After Carbon Ion Irradiation in BMSCs

作者：Zhang, Li-Ying[1];Yong, Wen-Xing[2];Wang, Lei[1];Zhang, Li-Xin[1];Zhang, Yi-Ming[1];Gong, Hong-Xia[1];He, Jin-Peng[3,4];Liu, Yong-Qi[1]

第一作者：张利英

通信作者：Liu, YQ[1]

机构：[1]Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Prevent &, 35 Dingxi East Rd, Lanzhou 730000, Gansu, Peoples R China;[2]Gansu Univ Chinese Med, Affiliated Hosp, Lanzhou 730000, Gansu, Peoples R China;[3]Chinese Acad Sci, Inst Modern Phys, Key Lab Space Radiobiol Gansu Prov, Lanzhou 730000, Gansu, Peoples R China;[4]Chinese Acad Sci, Inst Modern Phys, Key Lab Heavy Ion Radiat Biol & Med, Lanzhou 730000, Gansu, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Prevent &, 35 Dingxi East Rd, Lanzhou 730000, Gansu, Peoples R China.|[10735]甘肃中医药大学;

年份：2019

卷号：47

期号：3

起止页码：595

外文期刊名：AMERICAN JOURNAL OF CHINESE MEDICINE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000468960700007)】；

基金：This study was supported by the National Natural Science Foundation of China (Nos. 81473457 and 81660730); Collaborative Innovation Project of Chinese and Tibetan Medicine (No. XBXT2015-1), Project of Gansu Provincial Education Department (No. 2015A-095) and Project of Lanzhou Municipal Science and Technology Bureau (No. 2015-2-48).

语种：英文

外文关键词：BMSCs; Bystander Effect; Astragalus Polysaccharide; MAPK; TGF-beta

摘要：Although Astragalus polysaccharide (APS) has been shown to have various pharmacological effects, there have been no studies concerning the inhibitory effects of APS on the radiation-induced bystander effects (RIBE). The aim of this study was to investigate whether APS could suppress RIBE damage by inhibiting cell growth, micronucleus (MN) formation and 53BP1 foci number increased in bone marrow mesenchymal stem cells (BMSCs), named bystander cells, as well as to explore its mechanism. In this study, APS decreased proliferation and colony rate of bystander cells by inducing cell cycle arrest at G1 phase via extrinsic and intrinsic DNA damage. Regarding mechanism, APS inhibited mitogen-activated protein kinase (MAPK) signal pathway by down-regulating the expression of the key proteins, phosphorylated JNK (p-JNK), phosphorylated ERK (p-ERK) but not phosphorylated P38 (p-P38), and down-regulating their downstream function protein and molecule, cyclooxygenase-2 (COX-2) and reactive oxygen species (ROS). Moreover, in by-stander cells, APS inhibits expression of transforming growth factor beta receptor II (TGF-beta RII), a cell membrane receptor, resulting in lower ROS production and secretion via TGF-beta R-JNK/ERK-COX-2/ROS not P38 signaling. They gave a hint that the decreased RIBE damage induced by APS treatment involved TGF-beta R-JNK/ERK-COX-2/ROS down-regulation.