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

Figure 2

mTOR pathway 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) The markers of autophagy (LC3), apoptosis (procaspase-3, PARP), AMPK (AMPK-P), and mTOR (4-EBP1-P) were followed by immunoblotting. GAPDH was used as loading control. (b) Densitometry data represent the intensity of procaspase-3, cleaved PARP normalized for GAPDH, LC3II normalized for LC3I, AMPK-P normalized for total level of AMPK, and 4-EBP1-P normalized for total level of 4-EBP1. 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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