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Effects of cell growth and apoptosis of preneoplastic Syrian hamster embryo cells by green tea constituent epigallocatechin-3-gallate / 中华预防医学杂志
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-270486
Responsible library: WPRO
ABSTRACT
<p><b>OBJECTIVE</b>The co-culture model of Syrian hamster embryo (SHE) normal (primary cell) and preneoplastic cells mimicking in vivo status was established and used to study the chemopreventive effects of epigallocatechin-3-Gallate (EGCG) on cell growth, proliferation, apoptosis and regulated genes expression of SHE preneoplastic cells and discussed on the mechanism of EGCG's chemopreventive effect of carcinogenesis.</p><p><b>METHODS</b>The SHE cell preneoplastic and normal cells were cultured on the plates with 110,000, 11000, 1100, 110 rates for 7 days, and the co-culture model was established. The different concentration of EGCG (0, 0.5, 1, 5, 10, 50 micromol/L) were used to treat the cells and the SHE cells growth assay, in situ cell apoptosis assay, in situ cell proliferation assay and microarray assay were used to determined the growth, apoptosis and proliferation of SHE preneoplastic cells.</p><p><b>RESULTS</b>The co-culture model of SHE cells with the 1100 rate between SHE preneoplastic cells and normal cells was established. 0.5, 1, 5, 10 micromol/L EGCG increased the colony growth and proliferation of SHE normal cells. In the coculture model of SHE cells with 1200 rate, compared the the control group, 5, 10 micromol/L EGCG suppressed the growth of different size of SHE preneoplastic cells clone. The DNA proliferation index and apoptosis index in the control group were 39.3% and 6.5%, respectively. After treatment of 5, 10 micromol/L EGCG, the proliferation index were decreased to 25.6% and 24.8%, and the apoptosis index were increased to 12.65% and 14.5%. EGCG suppressed the growth and proliferation of SHE preneoplastic cells in co-culture model and increased its apoptosis. The pathway of cell apoptosis was regulated through the P53, NF-kappaB, bcl-2 signal pathway, and the pathway of cell proliferation was regulated through the growth arrest at G1/S phase of cell cycle.</p><p><b>CONCLUSION</b>The selective regulation of EGCG to normal and preneoplastic cells, the interaction of EGCG, SHE normal cells and SHE preneoplastic cells in co-culture model indicate that the suppression of proliferation and induction of apoptosis of preneoplastic cells by EGCG might be the mechanism of green tea' s chemopreventive effects to tumorigenicity.</p>
Subject(s)
Full text: Available Health context: SDG3 - Target 3.4 Reduce premature mortality due to noncommunicable diseases Health problem: Ovary Cancer Database: WPRIM (Western Pacific) Main subject: Pharmacology / Precancerous Conditions / Tea / Catechin / Cell Division / Chemistry / Cricetulus / CHO Cells / Apoptosis / Cell Line, Tumor Limits: Animals / Pregnancy Language: Chinese Journal: Chinese Journal of Preventive Medicine Year: 2007 Document type: Article
Full text: Available Health context: SDG3 - Target 3.4 Reduce premature mortality due to noncommunicable diseases Health problem: Ovary Cancer Database: WPRIM (Western Pacific) Main subject: Pharmacology / Precancerous Conditions / Tea / Catechin / Cell Division / Chemistry / Cricetulus / CHO Cells / Apoptosis / Cell Line, Tumor Limits: Animals / Pregnancy Language: Chinese Journal: Chinese Journal of Preventive Medicine Year: 2007 Document type: Article
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