Ginsenoside Rg1 inhibits proliferation of vascular smooth muscle cells stimulated by tumor necrosis factor-α
Ginsenoside Rg1 inhibits proliferation of vascular smooth muscle cells stimulated by tumor necrosis factor-α
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DOI：
10.1111/j.1745-7254.2006.00331.x
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发表时间：
2006-08-01
影响因子：
8.2
通讯作者：
Wang, Sheng-qi
中科院分区：
文献类型：
--
作者：
Ma, Zeng-chun;Gao, Yue;Wang, Sheng-qi
目的：目的：研究抗肿瘤Rg 1对血管平滑肌细胞（VSMC）增殖的影响，并从蛋白质组学角度探讨抗肿瘤Rg 1的作用机制。蛋白质组学改变进行了分析，使用二维电泳和肽质量指纹图谱。结果：肿瘤坏死因子-α（TNF-α）处理后，VSMC增殖明显增强，而TNF-α Rg 1处理后，VSMC增殖呈剂量依赖性抑制。蛋白质组学分析表明，24个蛋白质点发生了变化，其中17个蛋白质点增加，7个蛋白质点减少。人参皂苷Rg 1可以恢复这些蛋白质的表达水平，至少部分地，未处理的细胞的基本水平。TNF-α处理后VSMC G蛋白偶联受体激酶、蛋白激酶C（PKC）-zeta、N-ras蛋白表达下降，细胞周期相关蛋白p21表达增加。结论：TNF-α抑制VSMC增殖可能与PKC-zeta和p21通路有关。
Aim: To investigate the proliferation of vascular smooth muscle cells (VSMC) affected by ginsenoside Rg1 and further explore the molecular mechanism of ginsenoside Rg1 using proteomics.Methods: The proliferation of VSMC was measured by MTS assay kit and flow cytometry. Proteomic alterations were analyzed using two-dimensional electrophoresis and peptide mass fingerprinting. Differential proteins found in proteomics were confirmed by RT-PCR.Results: The proliferation of VSMC was enhanced significantly after tumor necrosis fac-tor-alpha (TNF-alpha) treatment, and ginsenoside Rg1 treatment inhibited proliferation in a dose-dependent manner. Proteomic analysis showed 24 protein spots were changed, including 17 spots that were increased and 7 spots that were decreased. Ginsenoside Rg1 could restore the expression levels of these proteins, at least partly, to basic levels of untreated cells. The expression of G-protein coupled receptor kinase, protein kinase C (PKC)-zeta, N-ras protein were decreased, while cycle related protein p21 was increased by ginsenoside Rg1 in TNF-alpha treated VSMC.Conclusion: PKC-zeta and p21 pathway might be the mechanism for inhibitory effects of ginsenoside Rg1 on proliferation of VSMC.