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中药复方得力生与Rg3及吉西他滨对HepG2细胞增殖抑制作用的比较

Antiproliferative Activity of the Chinese Medicinal Compound, Delisheng, Compared With Rg3 and Gemcitabine in HepG2 Cells.

作者信息

Wang S H, Wang Y C, Nie Y L, Hai Y N, Sun H F, Yuan Z L, Nan K J

机构信息

Department of Medical Oncology, The First Affiliated Hospital of The School of Medicine of Xian Jiaotong University, Xian, 710061, Shaanxi Province, P. R. China.

Center for Cell-Biological Therapy and Research, General Hospital of Guangzhou Millitary Command of PLA, Guangzhou, 510010, Guangdong Province, P. R. China.

出版信息

Indian J Pharm Sci. 2013 Sep;75(5):578-84.

Abstract

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.

摘要

得力生由人参、黄芪、蟾酥和斑蝥组成。据报道,得力生可抑制腺癌细胞增殖并诱导其凋亡。得力生还可增强机体免疫力并诱导癌细胞再分化。在MTT试验中,得力生抑制HepG2细胞增殖,且与人参提取物活性成分Rg3和吉西他滨相比,更有效地促进细胞凋亡。Rg3在得力生中可能起重要作用,因为它们均可调节细胞周期、细胞凋亡以及内皮抑素和VEGFR - 2的表达。在细胞周期分析中,得力生使细胞周期阻滞于S期,而吉西他滨使细胞阻滞于G0/G1期。因此,与单药相比,得力生联合吉西他滨可显著提高HepG2细胞系的凋亡率。与对照组相比,Western blot检测显示得力生组中procaspase蛋白、caspase蛋白和dr5的表达增加,而bcl - 2和survivin表达降低。这些观察结果表明,得力生诱导的凋亡效应可能与线粒体凋亡途径和死亡受体信号通路密切相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba3/3877520/4e6edc0c3c97/IJPhS-75-578-g001.jpg

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