Research Paper Volume 13, Issue 6 pp 8421—8439

PGC-1α alleviates mitochondrial dysfunction via TFEB-mediated autophagy in cisplatin-induced acute kidney injury


Figure 5. Activation of PGC-1α via ZLN005 inhibits cisplatin-induced mitochondria damage in vitro. (A) For the measurement of mitochondrial ROS (mtROS), HK2 cells were stained with Mito-SOX Red (2.5 μM) for 15 min at 37° C and determined by confocal microscope. Scar bar: 20 μm. (B) Mitochondrial ROS (mtROS) were measured by incubation with Mito-SOX Red. (C) The mitochondrial membrane potential measurement was detected with JC-1 (5 nM). Scar bar: 20 μm. (D) The expression of mitochondria-related proteins (ATP5b and Ndufs4) was measured by western blotting. (E) ATP content was measured by using an ATP Assay, ATP concentration was calculated in nmol/mg protein, and the data are represented as the rate of control. Data are provided as the mean ± SEM, n=3 independent experiments. *P < 0.05, **P < 0.01 vs. Con; &P < 0.05, &&P < 0.01, &&&P< 0.001 vs. Cisp. (Con, control; Zln, ZLN005; Cisp, cisplatin; C+Z, cisplatin + ZLN005).