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Chrysophanol protects against doxorubicin-induced cardiotoxicity by suppressing cellular PARylation.
Lu, Jing; Li, Jingyan; Hu, Yuehuai; Guo, Zhen; Sun, Duanping; Wang, Panxia; Guo, Kaiteng; Duan, Dayue Darrel; Gao, Si; Jiang, Jianmin; Wang, Junjian; Liu, Peiqing.
Afiliación
  • Lu J; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
  • Li J; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
  • Hu Y; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
  • Guo Z; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
  • Sun D; Guangzhou Key Laboratory of Construction and Application of New Drug Screening Model Systems, Guangdong Pharmaceutical University, Guangzhou 510006, China.
  • Wang P; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
  • Guo K; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
  • Duan DD; Laboratory of Cardiovascular Phenomics, Department of Pharmacology, University of Nevada Reno School of Medicine, Reno, NV 89557, USA.
  • Gao S; School of Medicine, Guangxi University of Science and Technology, Liuzhou 545005, China.
  • Jiang J; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
  • Wang J; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
  • Liu P; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
Acta Pharm Sin B ; 9(4): 782-793, 2019 Jul.
Article en En | MEDLINE | ID: mdl-31384538
The clinical application of doxorubicin (DOX) in cancer chemotherapy is limited by its life-threatening cardiotoxic effects. Chrysophanol (CHR), an anthraquinone compound isolated from the rhizome of Rheum palmatum L., is considered to play a broad role in a variety of biological processes. However, the effects of CHR׳s cardioprotection in DOX-induced cardiomyopathy is poorly understood. In this study, we found that the cardiac apoptosis, mitochondrial injury and cellular PARylation levels were significantly increased in H9C2 cells treated by Dox, while these effects were suppressed by CHR. Similar results were observed when PARP1 activity was suppressed by its inhibitors 3-aminobenzamide (3AB) and ABT888. Ectopic expression of PARP1 effectively blocked this CHR׳s cardioprotection against DOX-induced cardiomyocyte injury in H9C2 cells. Furthermore, pre-administration with both CHR and 3AB relieved DOX-induced cardiac apoptosis, mitochondrial impairment and heart dysfunction in Sprague-Dawley rat model. These results revealed that CHR protects against DOX-induced cardiotoxicity by suppressing cellular PARylation and provided critical evidence that PARylation may be a novel target for DOX-induced cardiomyopathy.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Acta Pharm Sin B Año: 2019 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Acta Pharm Sin B Año: 2019 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos