| Summary: | 碩士 === 國立中央大學 === 生命科學研究所 === 90 === Abstract
Obesity is considered as a common disease in the world and it is associated with the risks of diabetes, hypertension, and heart disease. Recent studies have shown that the body weight loss in rats and fatty acid energy expenditure in human are regulated by EGCG-containing green tea, but the exact mechanism of its action is still unclear. We here used a murine preadipose cell line 3T3-L1 to examine the mechanism at cellular and biochemical levels in the green tea regulation of fat cell growth. We found that green tea polyphenols reduced the cell number of 3T3-L1 preadipocytes. The IC50 for EGCG is about 20 µM, depending on the EGCG dosage and the developing status of the cells. EGCG-reduced cell number of 3T3-L1 preadipocytes may be due to the induction of growth arrest and apoptosis because this catechin increased the percentage of G2/M and sub-G1 phases of the cell cycle and caused the formation of DNA ladder. The growth arrest effect of EGCG may be associated with MAPK activity since a combination of EGCG and PD 098059 reduced the cell number of 3T3-L1 cells by 50-65 ﹪greater than that of PD 098059 alone. The apoptotic effect of EGCG could be caspase-3-dependent because EGCG increased caspase-3 activity and the effect of EGCG was blocked by caspase-3 inhibitor. There, we conclude that EGCG-induced growth in inhibition and apoptosis of 3T3-L1 preadipocytes may be related to the mechanism by which green tea reduces the body weight.
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