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Fig. 1 | Respiratory Research

Fig. 1

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

Fig. 1

Histological alterations in COPD smoker lungs. a Lungs from normal (nonsmokers), non-COPD smokers and COPD smokers stained with HE (100×). b, c, d MAST, MLI and DI in normal (nonsmokers), non-COPD smokers and COPD smokers. Non-COPD smokers did not show an emphysematous change, but had a thicker alveolar septum, MAST (μm), than nonsmokers (12.67 ± 2.00 vs. 7.78 ± 1.20, P < 0.01 by one-way ANOVA and LSD test). However, the COPD group had a thinner MAST (μm) than the nonsmoker group (5.00 ± 1.22 vs. 7.78 ± 1.20, P < 0.01 by one-way ANOVA and LSD test). COPD patients showed significant emphysematous disorder with a greater MLI (μm) and DI (%) than nonsmokers (213.33 ± 53.15 vs. 78.89 ± 23.69, P < 0.01 by Kruskal-Wallis test, and 76.22 ± 6.67 vs. 25.56 ± 4.67, P < 0.01 by one-way ANOVA and LSD test, respectively). *P < 0.05 vs. the nonsmoker group. Data in (b), (c), and (d) represent the means ± SD

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