Fig. 5

Neurotoxic damage involves oxidative stress and neuroinflammation in the auditory cortex. A, B DHE staining in brain coronal sections showing the auditory cortex (ACx) of control (A, Ctrl) and styrene-treated animals (B). C Histograms showing fluorescence intensity signal quantification. Data are expressed as mean ± SEM and are representative of three independent experiments from three animals/group. Scale bar: 100 μm. D, E Dot blots indicating an increase of protein tyrosine nitration (3-NT) and lipid peroxidation (4-HNE) in styrene-treated animals with respect to controls. d1, e1 Histograms (means ± SEM) show semi-quantitative analyses of optical density (3-NT, n = 4 animals for each group; Student’s t test, p = 0.003; 4-HNE, n = 4 animals for each group; Student’s t test, p = 0.016). Equal protein loading was assessed by Ponceau S staining. F–H Representative western blots showing high levels of inflammatory markers, such as IL-1β (F), COX-2 (G), NFκB and TNF-α (H). f1–h2 Graphs show the results of densitometric analyses on all samples for IL-1β (f1, n = 3 animals for each group; Student’s t test, p = 0.024), COX-2 (g1, n = 3 animals for each group; Student’s t test, p = 0.03), NFκB (h1, n = 4 animals for each group; Student’s t test, p = 0.0005) and TNF-α (h2, n = 4 animals for each group; Student’s t test, p = 0.001) normalized to the GAPDH or β-tubulin levels. Asterisks refers to significant differences between groups (*p < 0.05; **p < 0.01; ***p < 0.001)