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

Juan Chang,Huan Guo,Yingdong Li,Haiqiong Ran,Chengxu Ma,Guolian Chen,Youhua Wang

doi:10.1155/2021/5580828

Abstract

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-β1, Col1, and α-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.

Highlights

Radiation therapy (RT) is an essential treatment in the management of many malignancies
Radiation-induced myocardial fibrosis (RIMF) is the end stage of radiation-induced heart damage (RIHD) and contributes to all of these conditions. ere had previously found evidence of association; RIMF is mainly characterized by the proliferation of cardiac fibroblasts (CFs) and the synthesis and deposition of collagen, which are induced by a variety of cytokines and relative signaling pathways [6]
The quantity and lifespan of CFs become better than traditional methods. α-SMA actin and Vimentin as the standards [27] had identified the purity of CFs as showed in Figures 1(a) and 1(b). erefore, we performed this study’s in vitro model to evaluate whether low-dose radiation still causes the underlying damage for CFs

Summary

Introduction

Radiation therapy (RT) is an essential treatment in the management of many malignancies. A variety of degrees of damage can be produced after RT with an incidence as high as 20%–80% [1]. Oracic RT has been the most common application for treatment of Hodgkin’s lymphoma, breast cancer, lung cancer, esophageal cancer, and other malignancies in clinic practice [3, 4]. One of the major side effects of RT is RIHD (radiation-induced heart damage) that is inevitable due to the location of heart. Ere had previously found evidence of association; RIMF is mainly characterized by the proliferation of cardiac fibroblasts (CFs) and the synthesis and deposition of collagen, which are induced by a variety of cytokines and relative signaling pathways [6] RIMF (radiationinduced myocardial fibrosis) is the end stage of RIHD and contributes to all of these conditions. ere had previously found evidence of association; RIMF is mainly characterized by the proliferation of cardiac fibroblasts (CFs) and the synthesis and deposition of collagen, which are induced by a variety of cytokines and relative signaling pathways [6]

Methods

Results

Conclusion