Effect of total ginsenosides on the cell cycle of rat vascular smooth muscle cell proliferation induced by PDGF-BB

Aim To observe the effect of total ginsenosides(TG) on the cell cycle of rat vascular smooth muscle cell(VSMC) proliferation induced by platelet-derived growth factor-BB(PDGF-BB) and to probe especially into its mechanism. Methods VSMCs from the thoracic aorta of SD rats were cultured by tissue explant method. Effects of TG (10 mg·L-1,30 mg·L-1,100 mg·L-1) on PDGF-BB-induced VSMC proliferation were evaluated by MTT assay and the cell cycle was analyzed by flow cytometry. Expressions of endothelial NO synthase (eNOS),proto-oncogene c-fos (c-fos),CyclinD1 and P27 (KIP1) mRNA in VSMCs were detected by real-time quantitative reverse transcription-polymerase chain reaction(Real-time RT-PCR). Results TG 100 mg·L-1 had no effect on the growth and proliferation of normal VSMCs. PDGF-BB could significantly increase the absorbance of VSMCs in MTT assay (P0.01) and the percentage of S phase cells,and degrade the G0/G1 phase cell percentage in the cell cycle (P0.01). At the same time,PDGF-BB could up-regulate c-fos and CyclinD1 mRNA expressions,and down-regulate eNOS,P27(KIP1) mRNA expressions (P0.01). Addition of TG (10 mg·L-1,30 mg·L-1,100 mg·L-1) markedly inhibited the PDGF-BB-induced proliferation of the VSMCs,decreased the S phase cell percentage and upgraded the G0/G1 phase cell percentage in the cell cycle; TG could also depress the elevated expressions of c-fos and CyclinD1 mRNA induced by PDGF and up-regulate the expression of eNOS mRNA,but it had no effect on the mRNA level of P27(KIP1). Conclusions TG could inhibit the VSMC proliferation induced by PDGF-BB through preventing the transformation of the G0/G1 phase cell to S-phase cell in the cell cycle. The mechanisms may be related to its up-regulatory effect on eNOS mRNA and inhibition on C-fos and CyclinD1 mRNA expressions.