Histone deacetylase (HDAC) inhibitors have shown beneficial effects in animal models of cardiovascular diseases. We hypothesized that HDAC inhibitor, sodium valproate (VPA), has cardiac and vascular protective effects in rats with pressure overload cardiac hypertrophy induced by transverse aortic constriction (TAC). Sections of the heart were visualized after hematoxylin and eosin staining, picrosirius red staining and immunohistochemistry. The expression of genes related to cardiac hypertrophy, fibrosis, and oxidative stress was determined by quantitative real-time polymerase chain reaction. The aortic ring tension analysis was conducted using both the ascending aorta and descending thoracic aorta. TAC increased the expression of hypertrophic, fibrotic, and oxidative stress genes, which was attenuated by VPA. In the ascending aorta with intact endothelium, there was a significant decrease in the relaxation response, which was recovered by VPA treatment. These results indicate that VPA has cardiac and vascular protective effects in rats with pressure overload cardiac hypertrophy.
- MeSH
- Aorta surgery physiopathology drug effects MeSH
- Arterial Pressure drug effects MeSH
- Fibrosis MeSH
- Ventricular Function, Left drug effects MeSH
- Hypertrophy, Left Ventricular metabolism physiopathology pathology prevention & control MeSH
- Histone Deacetylase Inhibitors pharmacology MeSH
- Valproic Acid pharmacology MeSH
- Ligation MeSH
- Disease Models, Animal MeSH
- Myocardium metabolism pathology MeSH
- Oxidative Stress drug effects MeSH
- Rats, Sprague-Dawley MeSH
- Gene Expression Regulation MeSH
- Ventricular Remodeling drug effects MeSH
- Vasodilation drug effects MeSH
- Vasodilator Agents pharmacology MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
