Sophocarpine ameliorates cardiac hypertrophy through activation of autophagic responses
| Autor: | Huanliang Huang, Dong-Jian Huang, Jiong-Hua Huang, Yuebao Lin, Dexiong Chen |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Male animal structures Cardiomegaly 030204 cardiovascular system & hematology Pharmacology Applied Microbiology and Biotechnology Biochemistry Analytical Chemistry 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Alkaloids medicine Autophagy Animals Molecular Biology Sophora flavescens biology Ventricular Remodeling business.industry Angiotensin II Myocardium Organic Chemistry General Medicine biology.organism_classification Bioactive compound Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure chemistry Gene Expression Regulation Ventricle Cardiac hypertrophy Signal transduction business Function (biology) Biotechnology |
| Zdroj: | Bioscience, biotechnology, and biochemistry. 84(10) |
| ISSN: | 1347-6947 |
| Popis: | Mounting evidences indicate that autophagy is an essential homeostatic mechanism to maintain the global cardiac structure function. Sophocarpine (SOP), a major bioactive compound derived from the natural plant Sophora flavescens. However, the role of SOP in cardiac hypertrophy remain to be fully elucidated. In the present study, we tested the hypothesis that SOP protects against Ang II–induced cardiac hypertrophy by mediating the regulation of autophagy. The results demonstrated that SOP attenuated the Ang II–induced cardiac hypertrophy, as assessed by measurements of echocardiography parameters, the ratios of heart weight/body weight and left ventricle weight/body weight, histopathological staining, cross-sectional cardiomyocyte area, and the expression levels of cardiac hypertrophic markers. The anti-hypertrophic effect of SOP was mediated by activating autophagy-related pathway, as revealed by reversal of the increased autophagy marker protein expression. These findings reveal a novel mechanism of SOP attenuating cardiac hypertrophy via activating autophagy-related signaling pathways. |
| Databáze: | OpenAIRE |
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