Research Paper Volume 13, Issue 6 pp 8421—8439

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

Pharmacological activation of PGC-1α by ZLN005 treatment suppresses cisplatin-induced injury in vitro. HK2 cells treated with cisplatin (5 μM) were incubated with ZLN005 (10 μM) for 48 h. (A) cell viability was determined by CCK8 assay. (B) The expression of apoptosis-related proteins (Bax and Bcl-2) and PGC-1α was measured by western blotting. (C) The effects of ZLN005 on cisplatin-induced apoptosis were determined by flow cytometry. Data are provided as the mean ± SEM, n=3 independent experiments. *P &P

Figure 3. Pharmacological activation of PGC-1α by ZLN005 treatment suppresses cisplatin-induced injury in vitro. HK2 cells treated with cisplatin (5 μM) were incubated with ZLN005 (10 μM) for 48 h. (A) cell viability was determined by CCK8 assay. (B) The expression of apoptosis-related proteins (Bax and Bcl-2) and PGC-1α was measured by western blotting. (C) The effects of ZLN005 on cisplatin-induced apoptosis were determined by flow cytometry. Data are provided as the mean ± SEM, n=3 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 vs. Con; &P < 0.05 vs. Cisp. (Con, control; Zln, ZLN005; Cisp, cisplatin; C+Z, cisplatin + ZLN005).