| dc.description.abstract | Autophagy is a cellular process that protects the cell from stressful or starvation condition. This process requires a number of molecules that interact in a highly organized manner to help determine cell survival or death. Most polyphenols in green tea catechins, especially EGCG (epigallocatechin-3-gallate), act as an antioxidant and a regulator of fat cell activity. However, little information is known about the effect of EGCG on autophagy of fat cell. To fully understand whether EGCG regulates fat cell growth through regulation of autophagy, the role of EGCG in autophagy was investigated. EGCG was found to regulate a particular type of autophagy markers, such as Beclin-1, ATG3, ATG5, ATG7, ATG12-ATG5 conjugated, ATG16L1 proteins, as well as late autophagy markers (p62 and LC3B-II). In addition, 3-MA at 6 h tended to induce autophagy markers through ERK-independent pathway. Moreover, CQ was found to inhibit autophagy markers (Beclin-1, ATG3, ATG5, ATG7, ATG12-ATG5 conjugated, and ATG16L1) through different duration of treatment at 3 and 24 h, and then accumulated late phase markers (p62 and LC3B-II). Briefly, EGCG showed similar effect with CQ to modulate autophagy markers. Furthermore, EGCG time- and dose-dependently suppressed 3T3-L1 preadipocyte cell growth. Either in the presence of 3-MA (5 mM) or CQ (20 μM), it also suppressed 3T3-L1 preadipocyte cell growth. These findings indicate that EGCG might exert its anti-growth action through modulation of autophagy signaling protein. | en_US |