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Fig. 7 | Journal of Biomedical Science

Fig. 7

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

Fig. 7

TAKI-induced cell death exhibits the cell type specificity, and less susceptibility is not due to deficiency of TNF-α action. (a) RAW264.7, J774, BV-2, THP-1 monocyte, THP-1 macrophage differentiated by PMA (10 nM, 24 h), CHME3, DMVEC, CL1.0 and HeLa were treated with the indicated concentrations of TAKI for 6 h. Then LDH release to culture medium was measured. (b, c) In RAW264.7 and BV-2 cells, necrostatin-1 (Nec-1, 10 μM), enbrel (10 μg/ml) or zVAD (20 μM) was treated for 30 min before the administration of TAKI (100 nM) for 6 h. (d, e) A431, ARPE, HCT116 and NHEK cells were treated with TAKI (100 nM) and TNF-α (10 ng/ml) for 6 h. MTT (b, d) and ATP assays (c, e) were conducted to measure cell viability. *p <0.05, indicating significant cell death induced by TAKI. **p <0.05, indicating significant inhibition of TAKI-induced cell death by Nec-1, enbrel or zVAD. (f) TNFR protein expression in various cell types was compared by immunobloting

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