Fig. 6

Intrinsic autocrine action of TNF-α contributes the TAKI-induced cell death. (a) BMDM were pre-treated with enbrel (10 μg/ml), control IgG (1 μg/ml), TNF-α Ab (1 μg/ml) or IFN-Ab (1 μg/ml) for 30 min, and then treated with TAKI (100 nM) and/or LPS (100 ng/ml) for 6 h. Cell culture medium was used to determine LDH release. (b, c) BMDM were pre-treated with enbrel (10 μg/ml) for 30 min followed by TAKI and LPS for indicated intervals, and then cytosolic ROS (b) and mitochondrial ROS (c) were determined. (d) BMDM were treated with LPS (100 ng/ml), TAKI (100 nM) or both for indicated time intervials, and then the medium was collected to determine TNF-α production. *p <0.05, indicating significant effects of TAKI and/or LPS. #p <0.05, indicating significant inhibition of LPS-induced TNF-α release by TAKI (d) or significant enhancement of TAKI-induced LDH release by LPS (a). **p <0.05, indicating significant inhibition of TAKI- and/or LPS-induced responses by enbrel or TNF-α Ab