Jump to Main Content
Effects of Panax notoginseng saponins on proliferation and apoptosis of vascular smooth muscle cells
- Xu, Li, Liu, Jun-tian, Liu, Na, Lu, Pei-pei, Pang, Xiao-ming
- Journal of ethnopharmacology 2011 v.137 no.1 pp. 226-230
- Panax notoginseng, Western blotting, apoptosis, atherosclerosis, caspase-3, cell proliferation, flow cytometry, myocardial ischemia, myocytes, platelet-derived growth factor, protein synthesis, rats, saponins, smooth muscle, stroke
- AIM OF THE STUDY: Atherosclerosis is a common cardiovascular disease, and linked with the development of many cardiovascular complications, such as myocardial ischemia and stroke. Although pathogenesis of atherosclerosis is not completely elucidated, increasing evidence has demonstrated that abnormal proliferation of vascular smooth muscle cells (VSMCs) plays an important role in formation of atherosclerosis. Previous studies showed that saponins from Panax notoginseng (PNS) possess anti-atherosclerotic properties. However, the mechanism of PNS against atherosclerosis is not well understood. Therefore, the present study observed the effects of PNS on proliferation and apoptosis of VSMCs. MATERIALS AND METHODS: Rat VSMCs were cultured, and platelet-derived growth factor (PDGF) was used to stimulate cell proliferation. The viability of VSMCs was assessed with the MTT method. VSMCs apoptosis was detected by flow cytometry. Expressions of apoptosis related protein p53, Bax, caspase-3 and Bcl-2 were determined using Western blot. RESULTS: Pretreatment of the cells with PNS (200, 400, 800μg/mL) significantly inhibited proliferation of PDGF-stimulated VSMCs, and induced apoptosis of the proliferated VSMCs in a concentration-dependent way. Western blot analysis showed that PNS upregulated expressions of pro-apoptotic protein p53, Bax and caspase-3, downregulated expression of anti-apoptotic protein Bcl-2, and enlarged Bax/Bcl-2 ratio in the proliferated VSMCs induced by PDGF. CONCLUSIONS: This study demonstrates that PNS both inhibits VSMCs proliferation and induces VSMCs apoptosis through upregulating p53, Bax, caspase-3 expressions and downregulating Bcl-2 expression, which constitute the pharmacological basis of its anti-atherosclerotic action.