Study on the Inhibitory Effect of iQPR-H2O on A549 Cells

碩士 === 大仁科技大學 === 食品科技研究所 === 101 === Lung cancer has been currently become first leading cause of top ten cancers death in Taiwan. It’s of great urgency for us to develop more efficacious anticancer product. Water is the necessary drinks of organism for the daily life. In this study water via the I...

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Bibliographic Details
Main Authors: Man-Yu Chang, 張曼鈺
Other Authors: Den-En Shieh
Format: Others
Language:zh-TW
Published: 2013
Online Access:http://ndltd.ncl.edu.tw/handle/44423227573120105631
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Summary:碩士 === 大仁科技大學 === 食品科技研究所 === 101 === Lung cancer has been currently become first leading cause of top ten cancers death in Taiwan. It’s of great urgency for us to develop more efficacious anticancer product. Water is the necessary drinks of organism for the daily life. In this study water via the Infinitesimal Quantum Persistent Resources (iQPR) Technology treated was to evaluate the inhibitory effect and relative mechanism on human lung cancer cells (A549). A549 cells were cultured in medium prepared with iQPR-H2O or normal medium. MTT assay method was used to determine the inhibitory of iQPR-H2O on A549 cells, and 5-FU was used as a positive control drugs. As the results showed that the inhibition on A549 cells were better after treated with various ratio(10; 20; 30; 40; 50%)of iQPR-H2O for 8h, and the inhibitory was 60.16 ± 0.02; 57.78 ± 0.01; 53.83 ± 0.06; 51.66 ± 0.02; 59.10 ± 0.01%, respectively. Furthermore, 10% iQPR-H2O was not cytotoxic on MRC-5, a human normal lung cell. On the other hand, the cell cycle distribution of 10% iQPR-H2O treated A549 cells for 8h was determined by flow cytometry. The results demonstrate that cells were arrested at the G0/G1 phase(61.2%). Finally, 10% iQPR-H2O could regulate the expression of CDK4, CDK6, P15, P16, P53, caspase-3, but could not regulate the expression of Cyclin E1 and Caspase-9 on A549 cells by the western blotting analysis. Take together: iQPR-H2O exhibited significant anticancer activity through growth inhibition and protein regulation of CDK4, CDK6, P15, P53, caspase-3 and resulted in G0/G1 arrested as well as the induction of apoptosis on human lung cancer cells (A549).