| Summary: | 碩士 === 國立陽明大學 === 藥理學研究所 === 88 === Oral cancer is the 5th leading cause of death among all male cancer patients in Taiwan. Previous studies have clearly demonstrated a positive correlation between oral cancer and chewing betel quid. How to prevent and treat oral cancer is now becoming an important issue. Our laboratory found that areca nut extract could induce apoptosis in CHO-K1 cells. Recent report also indicated that (-)-epigallocatechin gallate (EGCG), an important polyphenolic component of green tea, could potentiate the cytotoxic potential of some drugs.
In the present study, human oral squamous cell carcinoma cell line OC2 were first treated with ripe areca nut extract (ANE) and different green tea polyphenols, such as catechin, (-)-epicatechin (EC), (-)-epicatechin gallate (ECG), (-)-epigallocatechin (EGC), and EGCG to evaluate their cytotoxic potential by the MTT assay. The result indicated that EGCG had obvious cytotoxic effect to OC2 oral cancer cells among all green tea polyphenol treated. Consequently, low dose EGCG (10 microM) and variable concentrations of ANE were studied on OC2 cells and analyzed by the MTT assay. The results demonstrated that EGCG enhanced the toxicity of ANE in a dose and time dependent manner in OC2 cells. This co-treatment of ANE 200 microg/ml and EGCG 10 microM induced apoptosis as evidenced by the cell morphology and DNA fragmentation analysis. The results also indicated that the combination of ANE 200 microg/ml and EGCG 10 microM induced oxidative damage to OC2 cancer cells as seen by the increase of 8-OH-dG. At the same time, DCF fluorescence was analyzed by flowcytometry, and it was found that the combination of ANE 200 microg/ml and EGCG 10 microM induced the formation of intracellular peroxides in OC2 cells. The above mentioned results demonstrated that EGCG potentiated the ANE-induced apoptosis in OC2 oral cancer cells, and this effect may be the result of increased production of peroxides and consequently the oxidative DNA damage in OC2 cells.
The effect of EGCG and ANE on normal cells was also investigated. The human epidermic cell line-HaCaT, an immortalized cell line, was chosen as the target cells. The results show that ANE (200 microg/ml) also induced apoptosis in HaCaT. However, the co-incubation of EGCG (10 microM) reduced the cytotoxic potential of ANE. The differential effects of EGCG in ANE-induced apoptosis in these two cell lines are not yet known and worthy of further investigation.
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