Authors

Yan Wan*, **, Weiwei Ouyang*, **, Shengfa Su*, **, Jun Zhang***, Qingsong Li*, **, Zhu Ma*, **, Yichao Geng*, **, Yan Yang*, **, Shilin Xu*, **, Bing Lu*, **, #

Departments

*Department of Oncology, Affiliated Hospital of Guizhou Medical University, Guiyang, PR China - **Teaching and Research Section of Oncology, Guizhou Medical University, Guiyang, PR China - ***Department of Pathology, Affiliated Hospital of Guizhou Medical University, Guiyang, PR China

Abstract

Objective: Radiation-induced heart disease (RIHD) is a concern during radiation therapy (RT). In past decades, recombinant human endostatin (rE) has widely been used for the treatment of non-small cell lung cancer. However, the incidence of rE-associated cardiovascular toxicity is substantial and previously under-recognised. 

Materials and methods: Sprague-Dawley rats were placed into the following experimental groups: RT (25Gy), rE (6mg/kg), rE (12mg/kg), RT (25Gy)+ rE (6mg/kg), RT (25Gy)+ rE (12mg/kg) and blank control groups. Hematoxylin and eosin staining (HE), Masson trichrome staining, Western blotting (TGF-β1, Smad2/3, collagen-I) and real-time PCR (TGF-β1, Smad2, Smad3, collagen-I) were performed to. 

Result: During autopsy, interstitial fibrosis could reliably be detected and quantified following irradiation and irradiation combined with recombinant endostatin hearts after follow-up times of 3 and 6 months. Based on Western blotting results, TGF-β1 and collagen-I was increased 3 and 6 months after irradiation and irradiation combined with recombinant endostatin on cardiac tissue. Real-time PCR results indicate that TGF-β1, Smad2, Smad3 and collagen-I increased 3 and 6 months after irradiation and irradiation combined with recombinant endostatin on cardiac tissue. 

Conclusion: The studied parameters could be used in future experiments for testing protective agents for the prevention of radiation heart injury and the toxicity of recombinant human endostatin.

Keywords

Radiation-induced heart disease (RIHD), recombinant human endostatin (rE), fibrosis, TGF-β1, Smad2/3, collagen-I.

DOI:

10.19193/0393-6384_2020_3_312