文献类型：期刊文献

英文题名：Ultrafiltration Extract of Radix Angelica Sinensis and Radix Hedysari Attenuates Risk of Low-Dose X-Ray Radiation-Induced Myocardial Fibrosis In Vitro

作者：Chang, Juan[1,2];Ma, Chengxu[3];Guo, Huan[4];Ran, Haiqiong[2];Chen, Guolian[2];Li, Yingdong[1]

第一作者：Chang, Juan

通信作者：Li, YD[1]

机构：[1]Gansu Univ Chinese Med, Coll Integrated Tradit Chinese & Western Med, Lanzhou 730000, Peoples R China;[2]Gansu Prov Hosp, Ctr Tradit Med Diag & Treatment, Lanzhou 730000, Peoples R China;[3]Lanzhou Univ, Dept Endocrinol, Hosp 1, 1 West Donggang Rd, Lanzhou 730000, Peoples R China;[4]Lan Zhou Univ, Sch Basic Med Sci, Lanzhou 730000, Peoples R China

第一机构：甘肃中医药大学中西医结合学院

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Coll Integrated Tradit Chinese & Western Med, Lanzhou 730000, Peoples R China.|[10735ed249c6606940a33]甘肃中医药大学中西医结合学院;[10735]甘肃中医药大学;

年份：2021

卷号：2021

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

收录：;Scopus(收录号：2-s2.0-85105717480);WOS:【SCI-EXPANDED(收录号:WOS:000655127100005)】；

基金：This work was supported by the National Natural Science Foundation of China (grant number 81873132).

语种：英文

摘要：The risk of radiation-induced heart damage (RIHD) is a growing concern since recent advances in radiation therapy (RT) for cancer treatments have significantly improved the number of survivors. Radiation-induced myocardial fibrosis (RIMF) is the final pathological condition of RIHD and main change leading to serious cardiovascular complications following RT. The aim of this study was to investigate the effect of ultrafiltration extract of Radix Angelica Sinensis and Radix Hedysari (RAS-RH) on the proliferation, apoptosis, and reactive oxygen species (ROS) of cardiac fibroblasts after X-irradiation in vitro. The RAS-RH extract was from the Danggui Buxue decoction (DBD) in TCM. Primary cardiac fibroblasts were irradiated with 1 Gy X-ray to evaluate the effect of RAS-RH on the expression levels of cell proliferation, apoptosis, ROS, and fibrotic molecules. Our data demonstrated that X-irradiation at 1 Gy resulted in the proliferation of cardiac fibroblasts; RAS-RH attenuated the myocardial fibrosis. Furthermore, X-ray radiation reduced the apoptosis of cardiac fibroblasts; RAS-RH accelerated the apoptosis of these cells after irradiation. In addition, the damage driven by ROS in primary cardiac fibroblasts after irradiation was weakened by RAS-RH and the expression of TGF-beta 1, Col1, and alpha-SMA increased after irradiation; RAS-RH decreased the expression of these makers. Overall, these data indicate that low-dose X-ray irradiation boosts myocardial fibrosis, and the effect of RAS-RH protects against fibrosis via attenuating the proliferation and accelerating the apoptosis of myocardial fibroblasts after X-irradiation.