Wei Zhang1, Gang Chen, Chang-Qing Deng. 1. Pathophysiology Laboratory, Hunan University of Traditional Chinese Medicine, Changsha, Hunan, China.
Abstract
OBJECTIVES: Total Panax notoginseng saponin (TPNS) is extracted from Panax notoginseng. Our previous studies suggested that TPNS could inhibit intimal hyperplasia. This study discussed the impact of TPNS on the proliferation of vascular smooth muscle cells (VSMCs) and revealed the associated mechanisms through cell cycle-related factors and extracellular regulated protein kinase (ERK) signal transduction pathway. METHODS: A VSMC proliferation model induced by platelet-derived growth factor (PDGF) was established to observe the effects of rat drug-containing plasma on VSMC proliferation. KEY FINDINGS: After being stimulated by PDGF, the proliferating cell nuclear antigen (PCNA) and c-fos content increased, while up-regulation of cyclinD1, cyclin-dependent kinase-4 (CDK4) and down-regulation of p21 protein were observed. These changes were inhibited by atorvastatin and TSPN drug-containing plasma, and the inhibitive activity in both groups was not significant. Furthermore, both atorvastatin and TSPN could obviously inhibit the activation of PDGF-induced P-ERK1/2 and increase the content of MKP-1, there were also no significant differences. CONCLUSIONS: These results suggested that atorvastatin and TPNS could inhibit VSMC proliferation by inhibiting the activation of ERK signalling pathway.
OBJECTIVES: Total Panax notoginsengsaponin (TPNS) is extracted from Panax notoginseng. Our previous studies suggested that TPNS could inhibit intimal hyperplasia. This study discussed the impact of TPNS on the proliferation of vascular smooth muscle cells (VSMCs) and revealed the associated mechanisms through cell cycle-related factors and extracellular regulated protein kinase (ERK) signal transduction pathway. METHODS: A VSMC proliferation model induced by platelet-derived growth factor (PDGF) was established to observe the effects of rat drug-containing plasma on VSMC proliferation. KEY FINDINGS: After being stimulated by PDGF, the proliferating cell nuclear antigen (PCNA) and c-fos content increased, while up-regulation of cyclinD1, cyclin-dependent kinase-4 (CDK4) and down-regulation of p21 protein were observed. These changes were inhibited by atorvastatin and TSPN drug-containing plasma, and the inhibitive activity in both groups was not significant. Furthermore, both atorvastatin and TSPN could obviously inhibit the activation of PDGF-induced P-ERK1/2 and increase the content of MKP-1, there were also no significant differences. CONCLUSIONS: These results suggested that atorvastatin and TPNS could inhibit VSMC proliferation by inhibiting the activation of ERK signalling pathway.