文献类型：期刊文献

英文题名：Huangqi Shengmai Yin Protects against Radiation-Induced Cardiac Fibrosis Injury by Regulating the TGF-1/Smads and MMPs

作者：Gu, Jing[1,2,3];Liu, Yongqi[1,3];Wu, Hongyan[3];Li, Hailong[3];Liu, Kai[3]

第一作者：顾静

通信作者：Liu, YQ[1];Liu, YQ[2]

机构：[1]Gansu Univ Tradit Chinese Med, Inst Integrated Tradit Chinese & Western Med, Lanzhou 730000, Gansu, Peoples R China;[2]Gansu Univ Tradit Chinese Med, Key Lab Transfer Dunhuang Med Prov & Ministerial, Lanzhou 730000, Gansu, Peoples R China;[3]Gansu Univ Tradit Chinese Med, 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 Tradit Chinese Med, Inst Integrated Tradit Chinese & Western Med, Lanzhou 730000, Gansu, Peoples R China;[2]corresponding author), Gansu Univ Tradit Chinese Med, Lanzhou 730000, Gansu, Peoples R China.|[10735]甘肃中医药大学;[10735ed249c6606940a33]甘肃中医药大学中西医结合学院;

年份：2019

卷号：2019

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

收录：;Scopus(收录号：2-s2.0-85066408655);WOS:【SCI-EXPANDED(收录号:WOS:000469193600001)】；

基金：We thank CureEdit for its linguistic assistance during the preparation of this manuscript. The work is supported by the National Natural Science Foundation of China (Grant no. 81660742), China Postdoctoral Science Foundation (Grant no. 2017M620477), and Scientific Research Project of Gansu Administration of Traditional Chinese Medicine (Grant no. GZK-2015-43).

语种：英文

摘要：Background. Radiation-induced heart damage is considered to be a progressive process of fibrosis. Emerging evidence has indicated that the Smads and matrix metalloproteinases (MMPs)/tissue inhibitors of MMPs (TIMP) may be involved in radiation-induced cardiac fibrosis (RICF) by regulating the activation of TGF-1 signaling pathway. Based on this, the present study was undertaken to characterize the effect of Huangqi Shengmai Yin (HSY) on RICF in a rat model. Methods. Precardiac region of rats was irradiated with 25Gy X-rays, and their myocardial pathology scores in terms of injury and collagen volume fraction (CVF) and the expression levels of fibrotic molecules were detected. Results. The pathology scores and CVF in myocardial tissue increased after irradiation, and the expression of TGF-1, Col1, and Col3 increased. This change indicated that such irradiation promoted the fibrosis damage in rat hearts. The damage was accompanied by an increase in the expression of Smad 2, Smad3, Smad4, and MMP14 and a decrease in the expression of Smad 7 and TIMP1. Administration of HSY weakened the RICF by decreasing pathology score and CVF and decreased the expression of TGF-1, Col1, and Col3 in irradiated rat hearts. In addition, Smad2, Smad3, Smad4, and MMP14 were downregulated, while Smad 7 and TIMP1 were upregulated during intervention with HSY. Conclusions. The involvement of the TGF-1/Smads and MMPs/TIMP system in RICF was confirmed. This study demonstrated, for the first time, that HSY attenuates the effects of RICF in a rat model. The effect HSY was found to be closely related to the TGF-1/Smads signaling pathway and MMPs system. These results suggest that HSY is a prospective drug for clinical treatment of RICF.