The effects of acrylonitrile on cell apoptosis, proliferation and related genes expression of rat normal and tumor glial cells / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study the effect of acrylonitrile (ACN) to cell growth, apoptosis, proliferation and related gene expression of rat normal glial cells (DI TNC1) and tumor glial cells (C6).</p><p><b>METHODS</b>The concentration of ACN on DI TNC1 and C6 were 25, 50 and 75 microg/ml. For cell growth, proliferation and apoptosis assay, the treated time was 24 hours, for microarray assay, the treated time was 4 and 24 hours.</p><p><b>RESULTS</b>After treatment of DI TNC1 cell with 25,50 and 75 microg/ml ACN, the DNA synthesis index were decreased 93.1%, 81.3% and 74.9% as compared to control respectively, the apoptosis index was increased 118%, 122% and 143% as compared to controls respectively. The DNA synthesis and apoptosis indexes of C6 cell showed no change after treatment with ACN. The cell cycle and apoptosis pathway related genes, such as cyclin and p53, also showed changes after treatment with ACN.</p><p><b>CONCLUSION</b>ACN inhibited the cell proliferation of DI TNC1, induced the apoptosis of DI TNC1 and had no effect on cell proliferation and apoptosis of C6 cells, and the related regulation gene expression changes further confirmed the results.</p>

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

<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 1:10,000, 1:1000, 1:100, 1:10 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 1:100 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 1:200 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>