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Fig. 2 | Respiratory Research

Fig. 2

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

Fig. 2

Increased apoptosis and oxidative stress in COPD patient lungs. a TUNEL staining was conducted in lung tissue samples from normal (nonsmokers), non-COPD smokers and COPD patients (400×). b AI was accounted for in the normal (nonsmoker), non-COPD smoker and COPD groups. → the TUNEL-positive nuclei. Compared to that in the lungs of nonsmokers and smokers without COPD, the AI (%) was increased in the lungs of COPD patients (3.73 ± 1.57 and 3.99 ± 1.75 vs. 24.79 ± 5.95, P < 0.01 by Kruskal-Wallis test). Interestingly, there was no difference in pulmonary AI between the nonsmokers and smokers without COPD (P = 0.976 by Kruskal-Wallis test). c Increased oxidative stress in the lungs of COPD patients. The level of ROS (RFU) in tissues from COPD patients was higher than that in tissues from nonsmokers (12.84 ± 2.16 vs. 5.17 ± 1.33, P < 0.01 by one-way ANOVA and LSD test), indicating that there was a higher oxidant burden in COPD patients. In contrast, the smokers without COPD did not show a significant change in ROS levels (5.03 ± 1.44 vs. 5.17 ± 1.33, P = 0.861 by one-way ANOVA and LSD test). *P < 0.05 vs. the normal group. Data in (b) and (c) represent the means ± SD

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