Research Article

Epigallocatechin-3-Gallate (EGCG) Promotes Autophagy-Dependent Survival via Influencing the Balance of mTOR-AMPK Pathways upon Endoplasmic Reticulum Stress

Figure 3

ULK1 is essential for EGCG-dependent autophagy induction. HEK293T cells were treated with rapamycin (Rap—100 nM, 2 h), H-89 (2.5 μM, 2 h), and EGCG (20 μM, 24 h) without/with followed by Rap (100 nM, 2 h) or H-89 (2.5 μM, 2 h) addition. (a) Meanwhile, the relative number of viable cells was denoted. (b) The markers of autophagy (LC3, ULK-555-P) and apoptosis (procaspase-3, PARP) were followed by immunoblotting. GAPDH was used as loading control. (c) Densitometry data represent the intensity of procaspase-3, cleaved PARP, and ULK-555-P and total level of ULK1 normalized for GAPDH, LC3II normalized for LC3I, and ULK-555-P normalized for total level of ULK. For each of the experiments, three independent measurements were carried out. Error bars represent standard deviation, and asterisks indicate statistically significant difference from the control: ; .
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