ReferenceID 4650
Bakuchiol Alleviates Hyperglycemia-Induced Diabetic Cardiomyopathy by Reducing Myocardial Oxidative Stress via Activating the SIRT1/Nrf2 Signaling Pathway
Oxid Med Cell Longev
Bakuchiol (BAK), a monoterpene phenol reported to have exerted a variety of pharmacological effects, has been related to multiple diseases, including myocardial ischemia reperfusion injury, pressure overload-induced card
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Record Fields
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- Reference Id
- 4650
- Evidence Id
- 21240
- Core Evidence Id
- 21240
- Source Reference Id
- 2569
- Herb2 Reference Id
- HBREF003366
- Subject Paper Key
- HBIN017546_33062139
- Pubmed Id
- 33062139
- Doi
- 10.1155/2020/3732718
- Paper Title
- Bakuchiol Alleviates Hyperglycemia-Induced Diabetic Cardiomyopathy by Reducing Myocardial Oxidative Stress via Activating the SIRT1/Nrf2 Signaling Pathway
- Paper Abstract
- Bakuchiol (BAK), a monoterpene phenol reported to have exerted a variety of pharmacological effects, has been related to multiple diseases, including myocardial ischemia reperfusion injury, pressure overload-induced cardiac hypertrophy, diabetes, liver fibrosis, and cancer. However, the effects of BAK on hyperglycemia-caused diabetic cardiomyopathy and its underlying mechanisms remain unclear. In this study, streptozotocin-induced mouse model and high-glucose-treated cell model were conducted to investigate the protective roles of BAK on diabetic cardiomyopathy, in either the presence or absence of SIRT1-specific inhibitor EX527, SIRT1 siRNA, or Nrf2 siRNA. Our data demonstrated for the first time that BAK could significantly abate diabetic cardiomyopathy by alleviating the cardiac dysfunction, ameliorating the myocardial fibrosis, mitigating the cardiac hypertrophy, and reducing the cardiomyocyte apoptosis. Furthermore, BAK achieved its antifibrotic and antihypertrophic actions by inhibiting the TGF-beta1/Smad3 pathway, as well as decreasing the expressions of fibrosis- and hypertrophy-related markers. Intriguingly, these above effects of BAK were largely attributed to the remarkable activation of SIRT1/Nrf2 signaling, which eventually strengthened cardiac antioxidative capacity by elevating the antioxidant production and reducing the reactive oxygen species generation. However, all the beneficial results were markedly abolished with the administration of EX527, SIRT1 siRNA, or Nrf2 siRNA. In summary, these novel findings indicate that BAK exhibits its therapeutic properties against hyperglycemia-caused diabetic cardiomyopathy by attenuating myocardial oxidative damage via activating the SIRT1/Nrf2 signaling.
- Journal
- Oxid Med Cell Longev
- Publish Year
- 2020
- Experiment Subject
- mouse; high-glucose-treated cell model
- Experiment Type
- Clinical Experiment
- Phenotype Related
- Cardiac Hypertrophy; Diabetic Cardiomyopathy; Myocardial Fibrosis; Cardiac Dysfunction; Liver Fibrosis; Hyperglycemia-caused Diabetic Cardiomyopathy; Cancer; Diabetes; Myocardial Ischemia Reperfusion Injury
- Paper Title Cn
- Paper Title En
- Bakuchiol Alleviates Hyperglycemia-Induced Diabetic Cardiomyopathy by Reducing Myocardial Oxidative Stress via Activating the SIRT1/Nrf2 Signaling Pathway
- Bilingual Status
- semi_complete