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. Author manuscript; available in PMC: 2017 Oct 1.
Published in final edited form as: Free Radic Biol Med. 2016 Aug 3;99:167–178. doi: 10.1016/j.freeradbiomed.2016.08.003

Fig. 1.

Fig. 1

Inhibition of histone deacetylase (HDAC) suppresses Nox2 activity in immune cells. (A-B) Neutrophil-differentiated, HL-60 cells were treated with vehicle (DMSO) or different doses of the HDAC inhibitor, scriptaid, for long-term (24 h) or short term (30 min) inhibition, and superoxide production was measured using L-012 chemiluminescence. (C) Macrophages isolated from C57BL/6 and Nox2−/− mice were treated with vehicle (DMSO) or different doses of scriptaid for 24 h, and superoxide production was measured using L-012 chemiluminescence. (D-E) HL-60 cells and macrophages were treated with increasing concentrations of the structurally distinct HDAC inhibitors, SAHA, TSA or Valproic Acid (VPA) for 24 h. Superoxide production was measured using L-012 chemiluminescence. Data are expressed as means ± S.E., *P<0.05 versus vehicle. (n=4–6).