The anti-inflammatory, antioxidative, and antiarteriosclerosis activities of simvastatin along with its protective effects on the endothelium suggest that it may also have antiaging effects. The aim of this study was to investigate the antiaging effects of simvastatin as well as its effects on sirtuin 1 (SIRT1) expression in endothelial cells. Aged rats and human umbilical vein endothelial cells were treated with simvastatin in the presence and absence of oxidized low-density lipoprotein (OX-LDL). Aortic β-galactosidase staining was undertaken to determine senescence, and SIRT1 protein expression was evaluated using Western blot analysis. After simvastatin therapy, arterial endothelial cell aging was significantly reduced, and SIRT1 expression was significantly increased. The OX-LDL significantly accelerated the senescence of umbilical vein endothelial cells and decreased SIRT1 expression. The OX-LDL-induced downregulation of SIRT1 was blocked by simvastatin. Simvastatin treatment also reduced umbilical vein endothelial cell aging and increased SIRT1 expression.
This study was designed to investigate whether mimecan was involved in aortic hypertrophy induced by sinoaortic denervation in rats. 8 weeks after sinoaortic denervation, when compared to sham-operated rats, sinoaortic denervated rats exhibited aortic hypertrophy and down-regulation of mimecan. Through classic univariate correlation analysis, it was found that mimecan mRNA was negatively related to extent of aortic hypertrophy. Treatment of primary cultured vascular smooth muscle cells with the Ang II (1 μM), which was found locally increased in the aortae of sinoaortic denervated rats, resulted in a reduction of mimecan expression. In vitro, knockdown of mimecan in vascular smooth muscle cells promoted cell proliferation induced by 15% of fetal bovine serum or Ang II (1 μM). We concluded that down-regulation of mimecan was involved in aortic hypertrophy induced by sinoaortic denervation in rats.
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