Ginsenoside Rb3 inhibits angiotensin II-induced vascular smooth muscle cells proliferation

This study was designed to examine the effect of ginsenoside Rb3 on angiotensin (Ang) II-induced proliferation of cultured rat vascular smooth muscle cells (VSMCs). VSMCs proliferation was evaluated by [3H]Thymidine incorporation. The cell cycle was examined by flow cytometry. The expression of mRNA of proto-oncogene c-myc, c-fos and c-jun was observed by RT-PCR. Ginsenoside Rb3 had no effects on VSMCs proliferation in physiological condition. Ang II significantly increased the proliferation of VSMCs and the expression of mRNA of proto-oncogene c-myc, c-fos and c-jun. Ginsenoside Rb3 markedly inhibited Ang II-induced VSMCs proliferation. Concomitantly, ginsenoside Rb3 decreased cell cycle progression from G(0)/G(1) to S phase. Furthermore, ginsenoside Rb3 significantly attenuated the expression of mRNA of proto-oncogene c-myc, c-fos and c-jun. This study showed that ginsenoside Rb3 inhibited Ang II-induced VSMCs proliferation, at least in part by inhibiting Ang II-induced G(0)/G(1) to S phase transition and attenuating the expression of mRNA of c-fos, c-jun and c-myc. The findings may explain the beneficial effects of ginsenoside Rb3 in cardiovascular diseases, and it will be useful to develop prevention and therapeutics of cardiovascular diseases.