Effects and mechanisms of total Panax notoginseng saponins on proliferation of vascular smooth muscle cells with plasma pharmacology method
Effects and mechanisms of total Panax notoginseng saponins on proliferation of vascular smooth muscle cells with plasma pharmacology method
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血浆药理学法研究三七总皂苷对血管平滑肌细胞增殖的影响及机制
DOI：
10.1111/j.2042-7158.2011.01379.x
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发表时间：
2012-01-01
影响因子：
3.3
通讯作者：
Deng, Chang-Qing
中科院分区：
文献类型：
--
作者：
Zhang, Wei;Chen, Gang;Deng, Chang-Qing
目的从三七中提取三七总皂苷(TPNS)。我们以前的研究表明三七总皂苷可以抑制血管内膜的增殖。本研究从细胞周期相关因子和细胞外调节蛋白激酶(ERK)信号转导途径探讨三七总皂甙对血管平滑肌细胞(VSMC)增殖的影响，并从细胞外调节蛋白激酶(ERK)信号转导途径探讨其作用机制。方法建立大鼠VSMC增殖模型，观察含药血浆对VSMC增殖的影响。主要研究结果显示，在PDGF刺激下，VSMC增殖细胞核抗原(PCNA)和c-fos含量增加，细胞周期蛋白依赖性蛋白依赖性激酶4(CDK4)表达上调，p21蛋白表达下调。阿托伐他汀和TSPN含药血浆对上述变化均有抑制作用，但两组抑制活性均不明显。此外，阿托伐他汀和三七总皂甙均能明显抑制PDGF诱导的P-ERK1/2的激活，增加MKP-1的含量，两者无明显差异。结论阿托伐他汀和三七总皂甙可能通过抑制ERK信号通路的激活来抑制VSMC的增殖。
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.