Key result
Ginsenoside Rb3 markedly inhibited Angiotensin II-induced vascular smooth muscle cell proliferation, decreased cell cycle progression to S phase, and attenuated proto-oncogene mRNA expression.
Why the study?
Does ginsenoside Rb3 inhibit angiotensin II-induced proliferation in cultured rat vascular smooth muscle cells?
Does ginsenoside Rb3 inhibit angiotensin II-induced proliferation in cultured rat vascular smooth muscle cells?
Ginsenoside Rb3 inhibits Ang II-induced proliferation of vascular smooth muscle cells by arresting cell cycle progression and attenuating proto-oncogene expression, suggesting potential therapeutic value in cardiovascular diseases.
May support preclinical vascular disease models; leaves open clinical translation in hypertension or atherosclerosis.
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.
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Wang et al. (2010) studied Angiotensin II-induced vascular smooth muscle cell proliferation. Ginsenoside Rb3 vs. Angiotensin II alone / physiological condition was evaluated on Vascular smooth muscle cell proliferation, cell cycle progression, and proto-oncogene mRNA expression. Ginsenoside Rb3 markedly inhibited Angiotensin II-induced vascular smooth muscle cell proliferation, decreased cell cycle progression to S phase, and attenuated proto-oncogene mRNA expression.
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