Fig. 4: Inhibition of PERK decreases mitochondrial dysfunction induced by treatment of B16-F10 cells with P2Et. | Cell Death Discovery

Fig. 4: Inhibition of PERK decreases mitochondrial dysfunction induced by treatment of B16-F10 cells with P2Et.

From: Polyphenol-rich extract induces apoptosis with immunogenic markers in melanoma cells through the ER stress-associated kinase PERK

Fig. 4: Inhibition of PERK decreases mitochondrial dysfunction induced by treatment of B16-F10 cells with P2Et.The alternative text for this image may have been generated using AI.

B16-F10 cells were treated with P2Et IC50 or Vehicle for 24 h, and then cells were harvested and labeled with a MitoSOX Red (100 mM) or b Mitotracker Red (100 mM). Fold change was determined using MFI from P2Et treatment relative to the vehicle for both dyes. Evaluation of mitochondrial membrane potential (ΔΨm): c B16-F10 cells were pre-treated with GSK2606414 (5 µM) for 2 h and then treated with P2Et IC50 or vehicle for additional 24 h. Cells were harvested and labeled with DioC2(3), the gate to analyze was made over B16-F10 cells treated with 1 µM of carbonilcianuro-m-clorofenilhidrazona (CCCP) 5 min prior FACS. A representative histogram of DioC2(3) fluorescence is shown. d Percentage of DioC2(3) low cells expressed as mean ± SEM of three independent experiments is shown. e JC-1 staining analysis of SCR and PERK KO cells treated for 12 h with P2Et IC50 or vehicle, % of Jc-1 aggregates expressed as mean ± SEM of three independent experiments is shown. *P < 0.05; **P < 0.01; ***P < 0.001

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