fig1

Figure 1. Schematic illustration of role of HDACs in acute lung injury (ALI). HDAC inhibitors: Tubacin (N1-[4-[(2R,4R,6S)-4-[[(4,5-diphenyl-2-oxazolyl)thio]methyl]-6-[4-(hydroxymethyl)phenyl]-1,3-dioxan-2-yl]phenyl]-N8-hydroxy-octanediamide)^[19,70]; Panobinostat (NVP-LBH589)^[20]; Trichostatin A (TSA, 7-[4-(dimethylamino)phenyl]-N-hydroxy-4,6R-dimethyl-7-oxo-2E,4E-heptadienamide)^[20,64]; RGFP-966 ((2E)-N-(2-Amino-4-fluorophenyl)-3-[(2E)-1-(3-phenyl-2-propen-1-yl)-1H-pyrazol-4-yl]-2-propenamide)^[20]; Tubastatin A (N-hydroxy-4-[(1,2,3,4-tetrahydro-2-methyl-5H-pyrido[4,3-b]indol-5-yl)methyl]-benzamide)^[61,62]; CAY10603 (N-[4-[3-[[[7-(hydroxyamino)-7-oxoheptyl]amino]carbonyl]-5-isoxazolyl]phenyl]-1,1-dimethylethyl ester, carbamic acid)^[61,62]; Sodium Butyrate (butanoic acid sodium salt)^[63,64]; Valproic acid (VPA, 2-Propylpentanoic acid)^[65-67]; Vorinostat (Suberoylanilide Hydroxamic Acid, SAHA)^[68]. LPS: lipopolysaccharides; E.coli: Escherichia coli; I/R: ischemia-reperfusion; MLC: myosin light chain; TNF-α: tumor necrosis factor-α; CINC-1: cytokine-induced neutrophil chemoattractant-1; IL-1β: interleukin 1β; IL-6: interleukin 6; NO: nitric oxide; ICAM-1: intercellular adhesion molecule 1; NF-κB p65: nuclear factor kappa-B p65 subunit; MPO: myeloperoxidase