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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.