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

Figure 6

EGCG-dependent effect on mTOR-AMPK pathways rescues GADD34 inhibition with respect to TG-induced ER stress. HEK293T cells were pretreated with GB (5 μM, 1 h) then without/with EGCG (20 μM, 24 h) followed by TG addition (10 μM, 2 h). The GB level was kept high until the end of the cell treatment. (a) After TG treatment, the markers of autophagy (LC3, ULK-555-P), apoptosis (procaspase-3, PARP), AMPK (AMPK-P), and mTOR (4-EBP1-P), as well as ER stress markers (eiF2α-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, ULK-555-P normalized for total level of ULK1, AMPK-P normalized for total level of AMPK, 4-EBP1-P normalized for total level of 4-EBP1, and eiF2α-P normalized for total level of eiF2α. 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: ; .

(a)

(b)