The effects of Radix Angelica Sinensis and Radix Hedysari ultrafiltration extract on X-irradiation-induced myocardial fibrosis in rats
Autor: | Huan Guo, Zhaoyuan Fu, Chengxu Ma, Huiping Wei, Xinke Zhao, Yingdong Li |
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Rok vydání: | 2019 |
Předmět: |
Male
0301 basic medicine Angelica sinensis MicroRNA-21 Cardiac fibrosis Ultrafiltration RM1-950 Pharmacology Radiation-induced myocardial fibrosis 03 medical and health sciences 0302 clinical medicine Fibrosis medicine Animals Osteopontin Rats Wistar Cells Cultured Radix Angelica Sinensis and Radix Hedysari ultrafiltration extract Dose-Response Relationship Drug biology Chemistry X-Rays Fabaceae General Medicine Total body irradiation Endomyocardial Fibrosis medicine.disease biology.organism_classification Rats Radiation Injuries Experimental Treatment Outcome 030104 developmental biology Apoptosis 030220 oncology & carcinogenesis biology.protein Transcription factor AP-1 Myocardial fibrosis Therapeutics. Pharmacology Drugs Chinese Herbal Transforming growth factor |
Zdroj: | Biomedicine & Pharmacotherapy, Vol 112, Iss, Pp-(2019) |
ISSN: | 0753-3322 |
DOI: | 10.1016/j.biopha.2019.01.057 |
Popis: | Radix Angelica Sinensis and Radix Hedysari are traditional Chinese medicines that are used for preventing and treating various diseases. This study aimed to investigate the effect and possible underlying mechanisms of Radix Angelica Sinensis and Radix Hedysari ultrafiltration extract (RAS-RH) on X-irradiation-induced cardiac fibrosis in rats. Our data demonstrated that (a) a single dose of total body irradiation (TBI) at 8 Gy resulted in cardiac fibrosis, whereas the control hearts exhibited less collagen and fibrosis. RAS-RH mitigated these morphological injuries. (b) TBI resulted in an increase in the serum levels of transforming growth factor β1 (TGF-β1) and troponin-I (TnI). RAS-RH inhibited the release of TBI-induced serum TGF-β1 and the TnI levels. (c) TBI inhibited the apoptosis of primary rat cardiac fibroblasts, whereas RAS-RH induced the apoptosis of primary rat cardiac fibroblasts after X- irradiation. (d) TBI resulted in an increase in the expression of osteopontin (OPN), c-fos, c-jun, miRNA-21 and collagen1α (COL1α) in primary rat cardiac fibroblasts, and RAS-RH mitigated the TBI-induced increased expression of OPN, c-jun, miRNA-21 and COL1α. In conclusion, these results demonstrate that RAS-RH exerts antifibrotic effects possibly through inducing the apoptosis of fibroblasts, inhibiting the release of serum TGF-β1, reducing the levels of serum TnI and reducing the expression of OPN, c-jun, miRNA-21 and COL1α. Therefore, RAS-RH may potentially be developed as a medical countermeasure for the mitigation of radiation-induced myocardial fibrosis. |
Databáze: | OpenAIRE |
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