Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

Oct 6, 2016Genetics and molecular research : GMR

Ginsenoside Rg1’s effects on aging in blood vessel muscle cells

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Abstract

Ginsenoside Rg1 significantly reduced the proportion of senescent vascular smooth muscle cells (VSMCs) compared to the D-galactose group.

D-galactose treatment increased the number of senescent VSMCs, as indicated by a rise in b-galactosidase-positive cells.
Ultrastructural changes in VSMCs were observed after D-galactose treatment.
The expression of cell cycle regulators p16, p21, and p53 was significantly elevated in the D-galactose group.
Rg1 treatment led to a significant decrease in senescent VSMCs and reduced levels of p16, p21, and p53 expression.
Cell cycle arrest in the G0/G1 phase was less pronounced in Rg1-treated cells compared to those treated with D-galactose.

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The development of age-related cardiovascular disease is associated with the senescence of vascular cells. This study aimed to investigate the effect of ginsenoside Rg1 on vascular smooth muscle cell (VSMC) senescence. Primary VSMCs were cultured and divided into control, D-galactose (D-gal), Rg1-L, and Rg1-H groups, which were cultured without and with D-gal, and with low- and high-concentrations of Rg1, respectively. D-gal-induced cellular senescence was identified by b-galactosidase staining, and ultrastructural changes within the cells were observed. The expression of p16, p21, and p53 in the four groups of VSMCs was determined by western blotting, and the cell cycle was investigated by flow cytometry. Compared with the control group, there was an obvious change in the ultrastructure of VSMCs in the D-gal group, and the proportion of b-galactosidase-positive cells was significantly increased (P < 0.05). In addition, p16, p21, and p53 expression was significantly increased (P < 0.05) and the cell cycle was arrested in the G0/G1 phase. Compared with the D-gal group, the percentage of positive cells was significantly reduced (P < 0.05) in the Rg1 groups, the expression of p16, p21, and p53 was significantly reduced (P < 0.05), and the number of cells in the G0/G1 phase decreased (P < 0.05). Ginsenoside Rg1 can inhibit VSMC senescence, and the mechanisms may be related to its partial inhibition of the p16/Rb and p53-p21signaling pathways during the cell cycle. INK4a Cip1/Waf1

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Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

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