文献类型：期刊文献

英文题名：The effects of Radix Angelica Sinensis and Radix Hedysari ultrafiltration extract on X-irradiation-induced myocardial fibrosis in rats

作者：Ma, Chengxu[1];Fu, Zhaoyuan[2];Guo, Huan[3];Wei, Huiping[2];Zhao, Xinke[2];Li, Yingdong[1]

第一作者：Ma, Chengxu

通信作者：Li, YD[1]

机构：[1]Gansu Univ Chinese Med, Coll Integrated Tradit Chinese & Western Med, 5 Dingxi East Rd, Lanzhou 730000, Gansu, Peoples R China;[2]Gansu Univ Chinese Med, Affiliated Hosp, Lanzhou 730000, Gansu, Peoples R China;[3]Lan Zhou Univ, Sch Basic Med Sci, Lanzhou 730000, Gansu, 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, 5 Dingxi East Rd, Lanzhou 730000, Gansu, 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：2019

卷号：112

外文期刊名：BIOMEDICINE & PHARMACOTHERAPY

收录：;Scopus(收录号：2-s2.0-85061532291);WOS:【SCI-EXPANDED(收录号:WOS:000461449400017)】；

基金：This work was supported by the National Natural Science Foundation of China (No. 81760798, 81873132).

语种：英文

外文关键词：Radix Angelica Sinensis and Radix Hedysari ultrafiltration extract; Radiation-induced myocardial fibrosis; MicroRNA-21; Osteopontin; Transcription factor AP-1

摘要：Radix Angelica Sinensis and Radix Hedysari are traditional Chinese medicines that are used for preventing and treating various diseases. This study aimed to investigate the effect and possible underlying mechanisms of Radix Angelica Sinensis and Radix Hedysari ultrafiltration extract (RAS-RH) on X-irradiation-induced cardiac fibrosis in rats. Our data demonstrated that (a) a single dose of total body irradiation (TBI) at 8 Gy resulted in cardiac fibrosis, whereas the control hearts exhibited less collagen and fibrosis. RAS-RH mitigated these morphological injuries. (b) TBI resulted in an increase in the serum levels of transforming growth factor beta 1 (TGF-beta 1) and troponin-I (TnI). RAS-RH inhibited the release of TBI-induced serum TGF-beta 1 and the TnI levels. (c) TBI inhibited the apoptosis of primary rat cardiac fibroblasts, whereas RAS-RH induced the apoptosis of primary rat cardiac fibroblasts after X-irradiation. (d) TBI resulted in an increase in the expression of osteopontin (OPN), c-fos, c-jun, miRNA-21 and collagen1 alpha (COL1 alpha) in primary rat cardiac fibroblasts, and RAS-RH mitigated the TBIinduced increased expression of OPN, c-jun, miRNA-21 and COL1 alpha. In conclusion, these results demonstrate that RAS-RH exerts antifibrotic effects possibly through inducing the apoptosis of fibroblasts, inhibiting the release of serum TGF-beta 1, reducing the levels of serum TnI and reducing the expression of OPN, c-jun, miRNA-21 and COL1 alpha. Therefore, RAS-RH may potentially be developed as a medical countermeasure for the mitigation of radiation-induced myocardial fibrosis.