Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add more filters










Database
Type of study
Language
Publication year range
1.
Cell Physiol Biochem ; 44(6): 2422-2438, 2017.
Article in English | MEDLINE | ID: mdl-29268252

ABSTRACT

BACKGROUND: Hypercholesterolemia is a risk factor for the development of cardiac hypertrophy. Astragaloside IV (AST-IV) possesses cardiovascular protective properties. We hypothesize that AST-IV prevents cardiac remodeling with hypercholesterolemia via modulating tissue homeostasis and alleviating oxidative stress. METHODS: The ApoE-/- mice were treated with AST-IV at 1 or 10 mg/kg for 8 weeks. The blood lipids tests, echocardiography, and TUNEL were performed. The mRNA expression profile was detected by real-time PCR. The myocytes size and number, and the expressions of proliferation (ki67), senescence (p16INK4a), oxidant (NADPH oxidase 4, NOX4) and antioxidant (superoxide dismutase, SOD) were observed by immunofluorescence staining. RESULTS: Neither 1 mg/kg nor 10 mg/kg AST-IV treatment could decrease blood lipids in ApoE-/- mice. However, the decreased left ventricular ejection fraction (LVEF) and fractional shortening (FS) in ApoE-/- mice were significantly improved after AST-IV treatment. The cardiac collagen volume fraction declined nearly in half after AST-IV treatment. The enlarged myocyte size was suppressed, and myocyte number was recovered, and the alterations of genes expressions linked to cell cycle, proliferation, senescence, p53-apoptosis pathway and oxidant-antioxidants in the hearts of ApoE-/- mice were reversed after AST-IV treatment. The decreased ki67 and increased p16INK4a in the hearts of ApoE-/- mice were recovered after AST-IV treatment. The percentages of apoptotic myocytes and NOX4-positive cells in AST-IV treated mice were decreased, which were consistent with the gene expressions. CONCLUSION: AST-IV treatment could prevent cardiac remodeling and recover the impaired ventricular function induced by hypercholesterolemia. The beneficial effect of AST-IV might partly be through regulating cardiac homeostasis and anti-oxidative stress.


Subject(s)
Apolipoproteins E/genetics , Cardiomegaly/drug therapy , Cardiotonic Agents/therapeutic use , Hypercholesterolemia/drug therapy , Oxidative Stress/drug effects , Saponins/therapeutic use , Triterpenes/therapeutic use , Ventricular Dysfunction, Left/drug therapy , Animals , Apoptosis/drug effects , Cardiomegaly/blood , Cardiomegaly/genetics , Cardiomegaly/pathology , Cardiotonic Agents/pharmacology , Female , Fibrosis , Gene Deletion , Hypercholesterolemia/blood , Hypercholesterolemia/genetics , Hypercholesterolemia/pathology , Lipids/blood , Male , Mice , Mice, Inbred C57BL , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/pathology , Saponins/pharmacology , Transcriptome/drug effects , Triterpenes/pharmacology , Ventricular Dysfunction, Left/blood , Ventricular Dysfunction, Left/genetics , Ventricular Dysfunction, Left/pathology
SELECTION OF CITATIONS
SEARCH DETAIL
...