Antiproliferative Activity of the Chinese Medicinal Compound, Delisheng, Compared With Rg3 and Gemcitabine in HepG2 Cells
Antiproliferative Activity of the Chinese Medicinal Compound, Delisheng, Compared With Rg3 and Gemcitabine in HepG2 Cells
复制标题
中药得力生与Rg3和吉西他滨抗HepG2细胞增殖活性比较
DOI：
10.4103/0250-474x.122879
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发表时间：
2013
影响因子：
0.5
通讯作者：
K. Nan
中科院分区：
文献类型：
--
作者：
S. H. Wang;Y. C. Wang;Y. Nie;Y. Hai;H. F. Sun;Z. Yuan;K. Nan
得力生由人参、黄芪、蟾酥、斑蝥组成。据报道，得力生可抑制腺癌细胞的增殖并刺激其凋亡。得力生还能增强机体免疫力，诱导癌细胞再分化。 MTT法检测得力生较人参提取物Rg3和吉西他滨活性成分更有效地抑制HepG2细胞增殖并促进细胞凋亡。 Rg3可能在得力生中发挥重要作用，因为它们都可以调节细胞周期、凋亡以及内皮抑素和VEGFR-2的表达。细胞周期分析中，得力生使细胞周期停滞在S期，而吉西他滨则将细胞阻滞在G0/G1期。因此，与单药相比，得力生联合吉西他滨可显着提高HepG2细胞系的凋亡率。 Western blot检测得力生组与对照组相比，procaspase蛋白、caspase蛋白、dr5表达升高，bcl-2、survivin表达降低。研究结果提示，得力生诱导细胞凋亡的作用可能与线粒体凋亡途径、死亡受体信号通路密切相关。
Delisheng consists of radix ginseng, radix astragali, venenum bufonis and mylabris. It has been reported that delisheng inhibits the proliferation of adenocarcinoma cells and stimulates their apoptosis. Delisheng can also enhance the body's immunity and induce the redifferentiation of carcinoma cells. Delisheng inhibited the proliferation of HepG2 cells in MTT assay and promoted apoptosis more effectively in contrast to the active components of ginseng extract, Rg3 and gemcitabine. It is possible that Rg3 has an important role in delisheng because they all could regulate the cell cycle, apoptosis and expression of endostatin and VEGFR-2. Delisheng caused the cell cycle to arrest at the S phase, while gemcitabine blocked the cells at the G0/G1 phase in cell cycle analysis. Consequently, the apoptosis rate of the HepG2 cell line can be increased significantly by delisheng in combination with gemcitabine, compared with the single drug. The expression of the procaspase proteins, caspase protein, and dr5 detected by Western blot were increased while bcl-2 and survivin decreased in the delisheng group, compared with controls. The observations suggest that the delisheng induced apoptotic effect might be closely related to the mitochondrial apoptosis pathway, and the death receptor signaling pathway.