ReferenceID 5981
Salidroside protects against cardiomyocyte apoptosis and ventricular remodeling by AKT/HO-1 signaling pathways in a diabetic cardiomyopathy mouse model
Phytomedicine
BACKGROUND: Diabetic cardiomyopathy is characterized by both systolic and diastolic dysfunction due to decreased contractility, as well as reduced compliance of the myocardium. Oxidative stress plays a significant role i
Relationship Network
Interactive first-hop connections across herbs, ingredients, formulas, targets, diseases, symptoms, syndromes, evidence, and monographs.
Click a node to open it in a new tab
Ingredient: 1Reference: 1Links: 1
Arranging relationship network...
Record Fields
Scalar fields from the final reference record.
- Reference Id
- 5981
- Evidence Id
- 22571
- Core Evidence Id
- 22571
- Source Reference Id
- 5226
- Herb2 Reference Id
- HBREF006023
- Subject Paper Key
- HBIN039698_33422954
- Pubmed Id
- 33422954
- Doi
- 10.1016/j.phymed.2020.153406
- Paper Title
- Salidroside protects against cardiomyocyte apoptosis and ventricular remodeling by AKT/HO-1 signaling pathways in a diabetic cardiomyopathy mouse model
- Paper Abstract
- BACKGROUND: Diabetic cardiomyopathy is characterized by both systolic and diastolic dysfunction due to decreased contractility, as well as reduced compliance of the myocardium. Oxidative stress plays a significant role in diabetes mellitus and its cardiovascular complications. Salidroside, a glucoside of the phenylpropanoid tyrosol, reportedly increases the levels of the antioxidative enzymes, nuclear factor erythroid 2-related factor 2, and heme oxygenase-1 (HO-1) to counteract oxidative stress; however, the underlying mechanisms are poorly understood. PURPOSE: Here we investigate the potential cardio-protective effects of salidroside and its mechanism in a diabetic animal model. METHODS: Male db/m, db/db, and age-matched wild-type mice were treated with salidroside at low dose (0.025 mg/kg) or high dose (0.05 mg/kg) by gavage every day for 12 weeks. Cardiac function and structure were assessed by echocardiography and histopathological examination. H9C2 cardiomyocytes were exposed in vitro to advanced glycosylation end products (400 mug/ml) and treated with salidroside (0.1, 1, or 10 muM). The expression of signaling-related genes were explored by western blotting and real-time PCR. RESULTS: Salidroside treatment significantly improved diabetes-induced cardiac dysfunction, hypertrophy, and fibrosis in vivo. Mechanistically, salidroside markedly up-regulates HO-1 expression by activation of the AKT signaling pathway. CONCLUSION: Salidroside protects against cardiomyocyte apoptosis and ventricular remodeling in diabetic mice. This cardio-protective effect of salidroside is dependent on AKT signaling activation.
- Journal
- Phytomedicine
- Publish Year
- 2021
- Experiment Subject
- mouse; h9c2 cardiomyocytes
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Diabetic Cardiomyopathy; Cardiovascular Complications; Diabetic; Cardiac Dysfunction; Diabetes Mellitus; Systolic And Diastolic Dysfunction; Fibrosis; Hypertrophy
- Paper Title Cn
- Paper Title En
- Salidroside protects against cardiomyocyte apoptosis and ventricular remodeling by AKT/HO-1 signaling pathways in a diabetic cardiomyopathy mouse model
- Bilingual Status
- semi_complete