The main pathological change in radiation-induced
heart disease is
fibrosis. Emerging evidence has indicated that
sodium tanshinone IIA sulfonate (STS) was used for treating fibrosis diseases. The present study was undertaken to characterize the effect of STS on radiation-induced cardiac
fibrosis (RICF) on cultured cardiac fibroblasts (CFs). CFs were irradiated with 1 or 2 Gy X-rays, and the expression of TGF-β1 and
collagen I (Col-1) increased, indicating that low-dose X-rays promoted
fibrosis damage effect. The
fibrosis damage was accompanied by morphologic changes in the endoplasmic reticulum (ER), as well as an increase in the expression of the ER stress-related molecules,
GRP78 and CHOP. Administration of STS reduced ROS production and decreased the expression of Col-1, TGF-β1, p-Smad2/3,
GRP78, and CHOP in irradiated CFs, thus weakening the
radiation-induced fibrosis damage and ER stress.
Radiation-induced fibrosis damage was observed on a cellular level. The involvement of ER stress in
radiation-induced fibrosis damage was demonstrated for the first time. STS attenuated the
fibrosis damage effect in CFs and this effect may be related to its
antioxidant action, and also related to its inhibition of ER stress and TGF-β1-Smad pathway. These results suggest that STS shows a good prospect in clinical prevention and treatment of RICF.