Effect of ginsenoside Rg3 on intimal proliferation and apoptosis of vascular smooth muscle cells after vascular injury in rats / 中草药

ABSTRACT

Objective: To investigate the effects of ginsenoside Rg3 on intimal proliferation and apoptosis of vascular smooth muscle cells after vascular injury in rats. Methods: Forty Sprague Dawley rats were divided into four groups randomly including Sham operation group, model group, ginsenoside Rg3 low-dose group (5 mg/kg), and ginsenoside Rg3 high-dose group (10 mg/kg). The carotid artery intima injury model was established by inflation balloons. From the next day after modeling, the rats were treated with ginsenoside Rg3 by ig administation in ginsenoside Rg3 groups, and rats in Sham operation group and model group were administered with same amount of normal saline. The injured common carotid arteries were harvested after 14 d and morphological changes of injured arteries were observed by HE staining. Terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) was used to detect the apoptosis of smooth muscle cells; Western blotting and qRT-PCR were used to detect the expression of Fas and anti-apoptotic gene Bcl-2. Results: Compared with the Sham operation group, the vascular neointima of rats in model group was significantly thicker, and the ratio of intima/media area and the apoptosis rate of neointimal hyperplasia were significantly increased. The expression of apoptosis-related gene Fas and anti-apoptotic gene Bcl-2 was significantly increased. Compared with model group, ginsenoside Rg3 (5 and 10 mg/kg) significantly alleviated vascular intimal hyperplasia, the intima/media area ratio and the expression of Bcl-2 was significantly decreased, and the apoptosis rate of smooth muscle cells in the neointimal area and the expression of Fas in injured vessels were significantly increased. Conclusion: Ginsenoside Rg3 can reduce the vascular neointimal hyperplasia induced by balloon injury with the possible underlying mechanism to promote the apoptosis of smooth muscle cells.