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. 2024 May 28;10:261. doi: 10.1038/s41420-024-02033-z

Fig. 5. RIPK3 is involved in Ru-TRZ-mediated cell damage.

Fig. 5

A Cell viability was evaluated in AML12 WT and Ripk3−/− cells after 24 h compound incubation (10 µM), using the AK release and MTS metabolism assays. B Mitochondrial ROS production was evaluated after 15 min compound incubation (10 µM) in AML12 WT and Ripk3−/− cells by fluorometric measurement of MitoSOX Red (580 nm). C Mitochondria transmembrane potential (ΔΨm) was evaluated by JC-1 staining of cells exposed to Ru-TRZ (10 µM) for 2 h or CCCP (200 µM) for 4 h (positive control) in AML12 WT and Ripk3−/− cells. DMSO is the vehicle control. Results are expressed as mean ± SEM fold-change to control, from at least three independent experiments. #p < 0.05 and §p < 0.001 from control vehicle-treated cells; *p < 0.05 from AML12 WT cells.