Reduction of the HIV Protease Inhibitor-Induced ER Stress and Inflammatory Response by Raltegravir in Macrophages
Figure 2
Effect of raltegravir on HIV PI-induced UPR activation in macrophages.
(A). Mouse J774A.1 cells were treated with different concentrations of raltegravir (0, 5, 15, 25 or 50 µM) in the absence or presence of ritonavir (RITV, 25 µM) or thapsigargin (TG, 100 nM), a known ER stress inducer, for 4 h, and the nuclear proteins were isolated. Representative immunoblots from three independent experiments for CHOP, XBP-1, ATF-4 and lamin B are shown. Lamin B was used as the loading control for nuclear proteins. (B). Human THP-1-derived macrophages were treated with different concentrations of raltegravir (0, 5, 15, and 25 µM) in the absence or presence of lopinavir/ritonavir (LOPV/RITV, 25 µM) for 4 h. Representative immunoblots from three independent experiments for CHOP, XBP-1, ATF-4 and lamin B are shown.