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. 2018 Sep 27;36:266–280. doi: 10.1016/j.ebiom.2018.09.031

Fig. 10.

Fig. 10

Celastrol ameliorated cisplatin-induced mitochondrial dysfunction in vitro.

(a) FACS analysis of mitochondrial ROS accumulation using MitoSOX™ Red Mitochondrial Superoxide Indicator in RTECs. RTECs were pretreated with celastrol, and then cultured with cisplatin (5 μg/mL) for 24 h. (b) qRT-PCR analysis of mtDNA in RTECs. 18 s was used as internal control. (c) Analysis of mitochondrial membrane potential (MMP) using JC-1 fluorescent probe in RTECs. (d-e) Seahorse 96xf detected basal oxygen consumption rate (OCR, representative of the basal mitochondrial OXPHOS activity) and spare respiratory capacity. Data were presented as means ± SD. n = 3 in each group. All experiments were duplicated for three times. Statistically significant differences were determined by one-way ANOVA, ## P < 0.01, ### P < 0.001, * P < 0.05, ** P < 0.01, *** P < 0.001.