Fig. 6

CS-induced oxidative stress is involved in the dysregulation of Bcl-2, cleaved caspase-3 and DNMT1 protein expression and the DNA hypermethylation of Bcl-2 promoter. a Immunoblotting was conducted in lungs from the control, CS exposure and CS exposure with Vit E treatment groups. b Densitometric analysis of Bcl-2 protein. Compared to the control group, the CS group exhibited decreased Bcl-2 protein level in the pulmonary tissue (0.62 ± 0.03 vs. 0.37 ± 0.05, P < 0.01 by one-way ANOVA and LSD test). However, the CS plus Vit E treatment group showed a Bcl-2 protein level similar to that of the control group (P = 0.10 by one-way ANOVA and LSD test). c The densitometric analysis of cleaved caspase-3. The expression of cleaved caspase-3 in the CS group was higher than that in the control group (0.75 ± 0.10 vs. 0.15 ± 0.05, P < 0.01 by Kruskal-Wallis test). In addition, the CS plus Vit E treatment group showed cleaved caspase-3 protein expression similar to that of the control group (P = 0.86 by Kruskal-Wallis test). d The densitometric analysis of DNMT1. Compared to the control group, the CS group had higher DNMT1 protein expression in the pulmonary tissue (0.18 ± 0.09 vs. 0.44 ± 0.10, P < 0.01 by Kruskal-Wallis test). In contrast, the CS plus Vit E treatment group showed DNMT1 protein expression similar to that of the control group (P = 0.96 by Kruskal-Wallis test). e DNA methylation level of the Bcl-2 promoter in the three groups. Compared to the control group, the CS group had increased Bcl-2 promoter methylation levels (%) in the lung (0.77 ± 0.94 vs. 3.25 ± 0.88, P < 0.01 by one-way ANOVA and LSD test). However, the CS plus Vit E treatment group showed a Bcl-2 promoter methylation level (%) similar to that of the control group (0.68 ± 0.67 vs. 0.77 ± 0.94, P = 0.79 by one-way ANOVA and LSD test). *P < 0.05 vs. the control group. The data in the figure represent the mean ± SD