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Figure caption:
Fig. 1. The mice with long-term CS exposure (presented as black dots) had gained body weight slower than the animals in the sham CS exposure group (presented as circles), a significant difference in body weight was noted from the 24th week (P < 0.05). Data presented as mean body weight ± SD (n = 10 in each group).
Fig. 2. Long-term cigarette smoke (CS) exposure induced emphysema-like pulmonary morphometry (panel A, 10×magnification), illustrated by a greater mean liner intercept (Lm) when compared to the sham CS exposure group (panel B, P < 0.05,). Two week course of treatment with roflumilast, pentoxifylline, theophylline or a combination of a glucocorticoid (Triamcinolone) with any of these phosphodiesterase inhibitors, did not mitigate pulmonary emphysema (panel B, P > 0.05).
Fig. 3. The expression of TNF-α (panel A) and IL-8 (panel B) in bronchoalveolar lavage fluid (BALF) samples was up-regulated by long term cigarette smoke (CS) exposure. Only PTX down-regulated the expression of TNF-α, while the addition of TRI did not increase this inhibition. PTX, THEO and TRI but not ROF down-regulated the expression of IL-8. The addition of TRI intensifies the inhibition, not only for PTX and THEO but also for ROF.
Results presented as mean ± SD (n = 5 mice for group).*P < 0.05, compared to the Sham-CS group;P < 0.05, compared to the CS group.
Fig. 4. Expression of ROS in the lung tissues was augmented by long-term CS-exposure (panel A, P < 0.05). PTX, THEO and TRI but not ROF inhibited ROS expression. The addition of TRI to ROF, however, increased the inhibition (panel B). the addition of TRI to PTX resulted in the synergistic inhibition on ROS expression (panel B, P < 0.05). Data presented as mean ± SD (n = 5 mice per group).*P < 0.05, compared to the Sham-CS group; P < 0.05, compared to the CS group; P < 0.05, compared to the CS+TRI group.
Fig. 5. The lungs having had long-term CS exposure had a greater reduction in HDAC-2 activity when compared to the lungs in the sham CS exposure group. ROF, PTX or THEO (but not TRI) partially restored HDAC-2 activity. The addition of TRI to each of the PDEIs, however, did not enhance HDAC-2 activity (P > 0.05). Data presented as mean ± SD (n = 5 mice for each group). *P< 0.05, compared to the Sham-CS; P< 0.05, compared to the CS group; P< 0.05, compared to the CS+TRI group.