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Fig. 8 | Respiratory Research

Fig. 8

From: Oxidative stress mediates the apoptosis and epigenetic modification of the Bcl-2 promoter via DNMT1 in a cigarette smoke-induced emphysema model

Fig. 8

DNMT1 gene silencing or pharmacologic inhibition ameliorates the CS-induced dysregulation of Bcl-2 and cleaved caspase-3 protein expression and hypermethylation of the Bcl-2 promoter. a Immunoblotting was conducted using lungs from the vector, CS + vector, CS + DNMT1 shRNA and CS + AZA groups. b Densitometric analysis of Bcl-2 protein. Compared to the CS group, the CS + DNMT1 shRNA and CS + AZA groups had higher Bcl-2 expression (0.24 ± 0.03 vs. 0.61 ± 0.05 and 0.59 ± 0.03, P < 0.01 by one-way ANOVA). c The densitometric analysis of cleaved caspase-3. There was less cleaved caspase-3 in the CS + DNMT1 shRNA and CS + AZA mice than in the CS mice (0.27 ± 0.05 and 0.19 ± 0.05 vs. 0.73 ± 0.04, P < 0.01 by one-way ANOVA). d The densitometric analysis of DNMT1. Compared to the CS group, the CS + DNMT1 shRNA and CS + AZA groups expressed less DNMT1 (0.60 ± 0.03 vs. 0.22 ± 0.05 and 0.31 ± 0.04, P < 0.01 by one-way ANOVA). e Methylation status of Bcl-2 promoter in the lungs from the four groups. Compared to the CS group, the CS + DNMT1 shRNA and CS + AZA groups had less Bcl-2 promoter methylation (%) in the lungs (3.95 ± 0.78 vs. 0.57 ± 0.60 and 0.47 ± 0.62, P < 0.01 by one-way ANOVA). These results indicate that DNMT1 gene silencing or inhibition prevented the downregulated Bcl-2 level, increased cleaved caspase-3 and hypermethylation in CS- exposed mice. *P < 0.05 vs. the CS group. The data in the figure represent the mean ± SD

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