Apocynin attenuates isoproterenol-induced myocardial injury and fibrogenesis
| Autor: | Minqi Xiong, Chenglin Jia, Qinbo Yang, Teng Zhang, Jingang Cui, Yu Chen, Li Li, Yu Xintong, Ning Bingbing, Peiwei Wang, Wenjian Wang, Xiaoye Du, Liu Li |
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| Rok vydání: | 2014 |
| Předmět: |
Male
Biophysics Inflammation Pharmacology medicine.disease_cause Biochemistry Antioxidants Pathogenesis Mice chemistry.chemical_compound Fibrosis Animals Humans Medicine Molecular Biology chemistry.chemical_classification Reactive oxygen species NADPH oxidase biology business.industry Isoproterenol Acetophenones Cell Biology Myocardial Disorder medicine.disease Mice Inbred C57BL Oxidative Stress Treatment Outcome chemistry Apocynin biology.protein Female medicine.symptom Cardiomyopathies Reactive Oxygen Species business Oxidative stress |
| Zdroj: | Biochemical and Biophysical Research Communications. 449:55-61 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2014.04.157 |
| Popis: | Oxidative stress is mechanistically implicated in the pathogenesis of myocardial injury and the subsequent fibrogenic tissue remodeling. Therapies targeting oxidative stress in the process of myocardial fibrogenesis are still lacking and thus remain as an active research area in myocardial injury management. The current study evaluated the effects of a NADPH oxidase inhibitor, apocynin, on the production of reactive oxygen species and the development of myocardial fibrogenesis in isoproterenol (ISO)-induced myocardial injury mouse model. The results revealed a remarkable effect of apocynin on attenuating the development of myocardial necrotic lesions, inflammation and fibrogenesis. Additionally, the protective effects of apocynin against myocardial injuries were associated with suppressed expression of an array of genes implicated in inflammatory and fibrogenic responses. Our study thus provided for the first time the histopathological and molecular evidence supporting the therapeutic value of apocynin against the development of myocardial injuries, in particular, myocardial fibrogenesis, which will benefit the mechanism-based drug development targeting oxidative stress in preventing and/or treating related myocardial disorders. |
| Databáze: | OpenAIRE |
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