The Investigation On The Inhibitory Proiferation Of Gastric Cancer Cell By G-rg1 And Its Mechanisms

Gastric cancer is one of the most common malignant tumor, malignant high,5-year survival rate, high incidence of distant organ metastasis, accounting for gastrointestinal cancer in China the first, third body tumor。The main methods for treating cancer, including surgery, chemotherapy, endoscopic therapy, radiotherapy, immunotherapy, gene therapy, enzyme and integrative Medicine treatment. Chinese medicine combined with chemotherapy for gastric cancer can reduce the toxicity caused by chemotherapy, to increase the efficacy of chemotherapy. With improving immunity and anticancer capacity, improve quality of life, side effects, easily the advantages for patients. Search for effective anticancer drug toxicity is the study of new anticancer drugs trend. Chinese traditional herbal medicine extracts for the development of low toxicity and high antitumor drugs provide a new way. Currently, more Chinese have studied ginseng, with Dai, berberine, garlic, astragalus, etc.. One widely used ginseng as a valuable medicine, with added vitality, soothe the nerves, Yifei, fluid, anti-aging and other effects。Araliaceae Panax ginseng is Panax Ginseng CAMey plant dry ginseng root。Body can be used as medicine. More pharmacological active ingredients of ginseng, including saponins, proteins, peptides, amino acids, organic acids, vitamins, fat soluble ingredients. Ginsenosides and ginseng polysaccharides as the main active ingredient, which ginsenoside Rgl (ginseno-side Rgl) are the main active ingredients of ginseng, has anti-tumor activity. But ginsenoside Rgl for anti-tumor mechanism is not very clear, this study Of ginsenoside Rgl on cultured BGC-823 of human gastric cancer cell inhibited proliferation and induced apoptosis and its mechanism. Main findings and conclusions were as follows:1 Study on the inhibitory proliferation of BGC-823 cells by G-Rgl. (1) MTT assay was used to investigate the inhibitory effect of G-Rgl on cultured BGC-823 cell proliferation. The results showed that,5ug/ml, 10ug/ml,20ug/ml,40ug/ml,80ug/ml Rgl, can inhibit cell proliferation, including the role of 80ug/ml strongest (2) morphology:light microscopy BGC-823 gastric cancer observed cells were polygonal or irregular in shape, adhered to the wall. The different concentrations of G-Rgl treated treatment group, the growth of many cells shed into the suspension state, the death of cancer cells in suspension more, smaller cells, cell refraction poor, dark cells, cells are more black granules With the increase of the concentration of the more obvious changes.80ug/ml G-Rgl 48h role of apoptosis began to change, cell suspension, the nuclei concentration. With the concentration and action time, number of apoptotic cells increased. Tip G-Rgl can directly inhibit the proliferation of BGC-823 cells.2 Study on the inhibitory proliferation from the regulation of cell cycle. Flow cytometry showed 20ug/ml G-Rgl treatment BGC-823 cells 48 hours after the Gl phase cell percentage increased from 58.25% to 67.27% P<0.01. The results showed that G-Rgl to cell growth arrest at G1/G0 period. Detected by RT-PCR of intracellular p16, p21 gene level. Gelimage analysis system found that 5ug/ml,20ug/ml,40ug/ml G-Rgl induced cell cycle inhibitor p16, p21 gene expression increased, and the action time with the change more apparent.Tip G-Rgl inhibited cell proliferation induced by cell differentiation and G-Rg1 G1 control the expression of cell cycle regulators of cell proliferation, blocked at the G1â†'S transition point. P16 protein was acting on the cell division cycle (Cell Division Cycle), one of the key enzyme inhibitor of CDK4. CDK (cyclin-dependent kinase) and cyclin (cyclin also known as loop elements) in the complex were not in the cell cycle phase at the same time play a role in DNA replication and induce starts mitosis, CDKS device may be the core of the cell cycle regulation. CDK4 and Cyclin complexes involved in G1-S transition control, p16 protein inhibits CDk4 activity, ultimately stopping cell into S phase.3 Study on the inhibitory proliferation from induced apoptosis by G-Rgl. Detected by flow cytometry after 5ug/ml,20ug/ml,40ug/ml G-Rgl for 72 hours, respectively BGC-823 gastric cancer cell apoptosis rate was 25.9%±0.1%,26.2%±11%and 41.40%±14.10% and the control group, the rate of apoptosis compared to 0.2%±0.1%increased significantly, and were dose dependent (P<0.01), whereas necrosis rates among groups compared with the control group no significant difference (P>0.05).In this study, ginsenoside Rgl on the inhibitory effect and mechanism of a number of experimental basic research, clinical ginsenoside Rg1 may provide some theoretical basis.