| dc.description.abstract | Abstract
Autophagy is a recycling process for protein aggregates, excess fat, and damaged mitochondria in cells. It protects the cells from stressful conditions (such as starvation and oxidative stress) and can be regulated by nutrients. EGCG, the major component of green tea catechins, has been known to act as a regulator of autophagy of cancer cells. But little information is known about the effect of EGCG on autophagy of fat cells. From our study, EGCG was found to suppress the cell growth in HIB1B brown preadipocytes after 12, 24, 36, and 48 hours of treatment in 0%, 2%, and 10% FBS, and was found to be dependent on the duration of treatment, the dose of EGCG, and the proportion of serum. Upon 12 hours of treatment, EGCG was observed to inhibit the initiation of autophagy as well as the degradation of autophagosomes in no to less serum conditions (0% and 2% FBS), but not in normal serum condition (10% FBS). In particular, EGCG altered the level of Atg3, Atg5, Atg7, Atg13, Atg16L1, LC3B-II/LC3B-I, pp62/p62, pAMPK, AMPK, pAKT, and AKT proteins in 0% FBS. And it altered the level of Atg7, Atg16L1, LC3B-II/LC3B-I, pp62/p62, pAMPK, pAKT, and AKT in 2% FBS. In 10% FBS, EGCG was found to alter Atg3, Atg7, LC3B-II/LC3B-I, and pp62/p62. Based on the puncta formation assay, EGCG was observed to decrease autophagy flux in 0% FBS, causing the cell to undergo an early phase autophagy suppression, but not in 2% and 10% FBS. Taken together, EGCG was found to inhibit the autophagy initiation (early phase of autophagy) through AMPK and autophagosome degradation (late phase of autophagy) in no serum condition (0% FBS). The increase presence of the serum seemed to decrease the effect of EGCG on autophagy. These findings suggest that the effect of EGCG on the autophagy process of HIB1B brown preadipocytes is dependent on the proportion of serum.
Keywords: Autophagy, EGCG, brown preadipocytes
| en_US |