(–)-Epicatechin Suppresses Angiotensin II-induced Cardiac Hypertrophy via the Activation of the SP1/SIRT1 Signaling Pathway
| Autor: | Ren-Jun Wang, Wei Han, Yuan-Qi Shi, Lin Wan, Zengxiang Dong, Xin Hai, Guangzhong Liu, Hui-Ling Hou, Sijia Zheng |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
medicine.medical_specialty
Angiotensin receptor Physiology Sp1 Transcription Factor Cardiomegaly 030204 cardiovascular system & hematology Catechin lcsh:Physiology lcsh:Biochemistry 03 medical and health sciences Mice 0302 clinical medicine SIRT1 Sirtuin 1 Internal medicine medicine Animals Myocytes Cardiac lcsh:QD415-436 Epicatechin lcsh:QP1-981 Chemistry Angiotensin II SP1 Cardiac hypertrophy Endocrinology 030220 oncology & carcinogenesis cardiovascular system Signal transduction hormones hormone substitutes and hormone antagonists Signal Transduction |
| Zdroj: | Cellular Physiology and Biochemistry, Vol 41, Iss 5, Pp 2004-2015 (2017) |
| ISSN: | 1421-9778 1015-8987 |
| Popis: | Background/Aims: Flavonol (–)-epicatechin (EPI) is present in high amounts in cocoa and tea products, and has been shown to exert beneficial effects on the cardiovascular system. However, the precise mechanism of EPI on cardiomyocyte hypertrophy has not yet been determined. In this study, we examined whether EPI could inhibit cardiac hypertrophy. Methods: We utilised cultured neonatal mouse cardiomyocytes and mice for immunofluorescence, immunochemistry, qRT-PCR, and western blot analyses. Results: 1µM EPI significantly inhibited 1µM angiotensin II (Ang II)-induced increase of cardiomyocyte size, as well as the mRNA and protein levels of ANP, BNP and β-MHC in vitro. The effects of EPI were accompanied with an up-regulation of SP1 and SIRT1, and were abolished by SP1 inhibition. Up-regulation of SP1 could block Ang II-induced increase in cardiomyocyte size, as well as the mRNA and protein levels of ANP, BNP and β-MHC, and increase the protein levels of SIRT1 in vitro. Moreover, 1 mg/kg body weight/day EPI significantly inhibited mouse cardiac hypertrophy induced by Ang II, which could be eliminated by SP1 inhibition in vivo. Conclusion: Our data indicated that EPI inhibited AngII-induced cardiac hypertrophy by activating the SP1/SIRT1 signaling pathway. |
| Databáze: | OpenAIRE |
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