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. Author manuscript; available in PMC: 2014 Jul 1.
Published in final edited form as: Free Radic Biol Med. 2013 Jan 29;60:233–245. doi: 10.1016/j.freeradbiomed.2013.01.025

Figure 8.

Figure 8

Proposed models demonstrating the different mechanisms by which mitochondria-targeted drugs, FCCP and antimycin A, and the classical antioxidants ebselen, DPI and MnTBAP, affect IL-1β secretion in mouse macrophages. (1) SAA stimulated mitochondria ROS to induce priming. When (2) ebselen and (2b) MnTBAP were added before SAA (top diagram), these drugs attenuated IL-1β secretion, perhaps due to their antioxidant activities against peroxide and mitochondrial ROS, respectively. On the other hand, (3) DPI enhanced IL-1β secretion associated with increases in intracellular ROS. (4) When mitochondrial-targeted drugs were added after SAA (bottom diagram), overproduction of mitochondrial ROS by FCCP or intracellular ROS by antimycin A or DPI was correlated with increases in IL-1β secretion. (4b) The robust effect of FCCP on IL-1β secretion was associated with sustained interaction among Nlrp3 inflammasome components; perhaps by decreasing their degradation. (5) After priming, MnTBAP appeared to exert its effects in increasing IL-1β secretion by a ROS independent mechanism.