Yanfang Wan, W. Ouyang, S. Su, Jun Zhang, Shi-Lin Xu, Zhu Ma, Qingsong Li, Y. Geng, B. Lu
{"title":"Mechanism of radiation combined with recombinant human endostatin in inducing myocardial fibrosis","authors":"Yanfang Wan, W. Ouyang, S. Su, Jun Zhang, Shi-Lin Xu, Zhu Ma, Qingsong Li, Y. Geng, B. Lu","doi":"10.3760/CMA.J.CN113030-20190911-00009","DOIUrl":null,"url":null,"abstract":"Objective \nThe experimental animal model was established to unravel the mechanism of radiation-induced myocardial fibrosis and validate the role of recombinant human endostatin in aggravating the process of radiation-induced myocardial fibrosis via the TGF-β 1, Smad2 and Smad3 signaling pathways. \n \n \nMethods \nSixty male adult Sprague-Dawley rats were randomly divided into the following groups: radiotherapy (RT)25 Gy, recombinant human endostatin (RE) 6 mg/kg, RE 12 mg/kg, RT 25 Gy+ RE 6 mg/kg, RT 25 Gy+ RE 12 mg/kg and blank control groups. Five rats were sacrificed in each group at 1 and 3 months after interventions. The myocardial tissues were collected. The pathological changes were observed by Hematoxylin and eosin staining. The degree of fibrosis was assessed by Masson trichrome staining. The expression levels of TGF-β1, Smad2, Smad3 and Collagen-I mRNA and protein were quantitatively measured by real-time PCR and Western blotting. \n \n \nResults \nAt 3 months after intervention, Masson trichrome staining revealed that the collagen deposition in the RT 25Gy and RT 25Gy+ RE (6 and 12 mg/kg) groups was more significant than that in the control group. In addition, The expression levels of TGF-β1, Smad2, Smad3 and Collagen-I mRNA and protein in these groups were significantly up-regulated compared with those in the control group. \n \n \nConclusions \nRadiation with a total physical dose of 25 Gy can induce myocardial fibrosis in the SD rat models. TGF-β 1 and Smad2 signaling pathways are the common signaling pathways of myocardial fibrosis induced by radiation combined with recombinant human endostatin. \n \n \nKey words: \nRadiation-induced heart disease; Recombinant human endostatin; TGF-β1 gene; Smad2 gene; Smad3 gene; Collagen-I gene","PeriodicalId":10288,"journal":{"name":"中华放射肿瘤学杂志","volume":"29 1","pages":"294-299"},"PeriodicalIF":0.0000,"publicationDate":"2020-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"中华放射肿瘤学杂志","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3760/CMA.J.CN113030-20190911-00009","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Objective
The experimental animal model was established to unravel the mechanism of radiation-induced myocardial fibrosis and validate the role of recombinant human endostatin in aggravating the process of radiation-induced myocardial fibrosis via the TGF-β 1, Smad2 and Smad3 signaling pathways.
Methods
Sixty male adult Sprague-Dawley rats were randomly divided into the following groups: radiotherapy (RT)25 Gy, recombinant human endostatin (RE) 6 mg/kg, RE 12 mg/kg, RT 25 Gy+ RE 6 mg/kg, RT 25 Gy+ RE 12 mg/kg and blank control groups. Five rats were sacrificed in each group at 1 and 3 months after interventions. The myocardial tissues were collected. The pathological changes were observed by Hematoxylin and eosin staining. The degree of fibrosis was assessed by Masson trichrome staining. The expression levels of TGF-β1, Smad2, Smad3 and Collagen-I mRNA and protein were quantitatively measured by real-time PCR and Western blotting.
Results
At 3 months after intervention, Masson trichrome staining revealed that the collagen deposition in the RT 25Gy and RT 25Gy+ RE (6 and 12 mg/kg) groups was more significant than that in the control group. In addition, The expression levels of TGF-β1, Smad2, Smad3 and Collagen-I mRNA and protein in these groups were significantly up-regulated compared with those in the control group.
Conclusions
Radiation with a total physical dose of 25 Gy can induce myocardial fibrosis in the SD rat models. TGF-β 1 and Smad2 signaling pathways are the common signaling pathways of myocardial fibrosis induced by radiation combined with recombinant human endostatin.
Key words:
Radiation-induced heart disease; Recombinant human endostatin; TGF-β1 gene; Smad2 gene; Smad3 gene; Collagen-I gene
期刊介绍：
The Chinese Journal of Radiation Oncology is a national academic journal sponsored by the Chinese Medical Association. It was founded in 1992 and the title was written by Chen Minzhang, the former Minister of Health. Its predecessor was the Chinese Journal of Radiation Oncology, which was founded in 1987. The journal is an authoritative journal in the field of radiation oncology in my country. It focuses on clinical tumor radiotherapy, tumor radiation physics, tumor radiation biology, and thermal therapy. Its main readers are middle and senior clinical doctors and scientific researchers. It is now a monthly journal with a large 16-page format and 80 pages of text. For many years, it has adhered to the principle of combining theory with practice and combining improvement with popularization. It now has columns such as monographs, head and neck tumors (monographs), chest tumors (monographs), abdominal tumors (monographs), physics, technology, biology (monographs), reviews, and investigations and research.
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