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Fig. 5 | Journal of Biomedical Science

Fig. 5

From: TAK1 inhibition-induced RIP1-dependent apoptosis in murine macrophages relies on constitutive TNF-α signaling and ROS production

Fig. 5

TAKI-induced cell death involves mitochondrial dysfunction. (a) BMDM were treated with 20 μM zVAD or 10 μM Nec-1 for 30 min, followed by TAKI (100 nM) and/or LPS (100 ng/ml) for 6 h. Then mitochondria membrane potential was detected. *p <0.05, indicating significant reduction of mitochondrial membrane potential caused by TAKI. **p <0.05, indicating significant potentiation or inhibiion of mitochondrial membrane potential loss by zVAD and Nec-1, respectively. (b) The mitochondrial metabolism was assessed by using the seahorse XF24 to measure the oxygen consumption rate (OCR). BMDM were treated with LPS (100 ng/ml), TAKI (100 nM), or LPS plus TAKI at 32 min as indicated with arrow. The inhibitor of ATP synthase, oligomycin (10 μg/ml) was added to discriminate ATP-linked respiration and proton leak. After adding an uncoupler of mitochondrial oxidative phosphorylation, FCCP (2.5 μM), OCR was raised to the maximal respiratory capacity. Finally rotenone (2.5 μM) was added to block the electron transport chain of oxidative phosphorylation

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