TAZ rescued the defects in ATP, mitochondrial O2−, and MMP via Nrf2
(A and B) TAZ resisted the disorder of ATP and mitochondrial O2− levels through Nrf2. After introduction of the TAZ overexpression plasmid, ATP (N = 9) and mitochondrial O2− (N = 3) levels were determined in the absence or presence of the Nrf2 inhibitor ML385 in the context of LPS. (C and D) TAZ improved the defective MMP via Nrf2. After treatment as outlined above, BV2 microglial cells were incubated with the JC-1 fluorescent probe or TMRM to analyze the change in MMP by flow cytometry or confocal microscopy in the context of LPS. N = 4.
Scale bar, 20 μm. Hoechst, Hoechst 33342.